Physiology

A Message from the Author

Dear Emerging Biologist,

Welcome to the word of Human Physiology. I remember the first time my passion for biology was awakened. There I was, sitting in my Physiology class in college and the first section was on the Nervous System. Wow, I was immediately amazed at the complexity of it all. Little tiny neurons, smaller than the human eye could see, with so much going on that we still cannot fully explain everything that’s going on in there.

However, there is one thing that I know. Many people struggle to understand some of the concepts because of how complex they are. That is the exact reason why you are reading this today. These notes are the result of some crazy typing during my physiology class, and many hours of work since then. When I took the class, I was determined to type as much of what my professor said, so that when it was time to study, I had EVERYTHING I needed in my notes. That was not my only motivating factor. I also wanted to be able to provide it as a resource for the other students in my class.

What happened next amazed me. Everyone in that class was using my notes. Not only that, but people who took the class years after are still using my notes today and letting me know how much it helped them to pass a class that they thought they would fail. To make it even better, I started getting people from different parts of the globe letting me know that my notes helping them in their classes. This really does my heart well. To think that something that I did so long ago (10+ years) can help so many people is just amazing.

So, I decided to spruce them up a little. I went through, made some structural changes, added some more content and images to help to make it even MORE helpful and the result is the ebook that you have before you. I’ll also be adding lots of content and resources on Interactive Biology to help you do even better, so be sure to visit often. In fact, I will be linking to videos that enhance the content all throughout this study guide. Whenever, you see the following icon (except this first one), you can click on it and go to the relevant video.

I really hope all of these resources help you not only pass your Physiology class, but pass with a HIGH A. My goal is to make it as easy for you as possible.

Happy Learning!

Leslie Samuelwww.Interactive-Biology.com

Human Physiology - By Leslie Samuel

Copyright © 2014, www.Interactive-Biology.com. Join The Academy. - Back to Table of Contents - 2 -

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Table of Contents

You may click any title to go directly to the section

The Types of Neurons p. 5 Visual Processing p.29

The Functions of Neurons p. 6 On Center, Off Surround Ganglion cells

p.30

Ion Channels p. 7 Phonoreception p.32

Donnan Equilibrium p. 8 The Muscular System p.35

The Na-K Pump p. 9 The Sliding Filament Theory p.37

V-gated ion channels p.10 Sarcomere Structure and Function

p.38

Conductance p.10 The Circulatory System p.40

The Nerve Impulse/Action Potential p.12 Control of the Heart Beat p.42

Refractory Periods p.12 Contraction of the Heart p.44

Conduction Velocity p.13 Regulating Stroke Volume p.44

The Synapse p.14 Regulating Cardiac Output p.45

Summation and facilitation p.16 Regulating Blood Pressure p.46

Neurotransmitters, agonists and antagonists

p.18 Regulating Peripheral Resistance

p.47

Organization of the Central Nervous System

p.19 The Cardiac Cycle p.50

Organization of the Brain p.21 Human Circulatory Difficulties p.52

Intellectual Functions and Sleep p.23 The Respiratory System p.54

The Sensory Nervous System p.25 The Oxygen Dissociation Curve p.56

Receptors p.25 The Human Respiratory System p.58

Photoreception p.26 Pressure changes during Respiration

p.59

Retinal Structure p.28







The Nervous System

The Nervous System

The Types of NeuronsThere are many different types of neurons (morphologies). In this section, we will deal with the general categories, starting with the one that is typically shown in textbooks. However, keep in mind that this is a simplified version that is illustrated to simply show the parts of a neuron. In real life, neurons deviate from this Classical Neuron significantly, but have the same general structures and characteristics.

The Multipolar Neuron (Classical Neuron): This neuron has one axon (which is typical of nerve cells, more axons are rare cases), and numerous dendrites. In this picture, the dendrites are the treelike arborization that comes from the soma. The axon terminals of the input are where the EPSPs and IPSPs originate.

Dendrites are the points of synaptic connections. Some synaptic connections are made with the soma and are "the same" as dendrite connections. Connections on the soma are usually the "stronger" connections. This axon is branching (typical).

The Soma is the part of the neuron that is most like other cells. It has the nucleus, genetic machinery, and is where many of the metabolic processes happen. However, mRNA molecules are sometimes targeted for a specific site for the release of neurotransmitter.

Neurons are among the most complex of cells. The Axon has a base where it is continuous with the soma. This swollen section is called the axon hillock, or the "spike" initiating zone (where the nerve impulse originates). This is the first region of the neuron with Voltage-gated (V-gated) ion channels. This is a requirement for a nerve impulse. When the nerve impulse begins, it travels down the axon. It then reaches the axon terminals, who's function is to release neurotransmitter, which then cause EPSPs and IPSPs in the following neuron (to be discussed later).

Other Morphologies

Unipolar: Has no dendrites. The synaptic connections are with the soma, who’s membrane functions as dendrites.Pseudounipolar: There is only one process coming off the soma but there are dendrites and axons (most common in the animal world - insects and invertebrates). There is a spike initiating zone but it isn't anatomically distinguishable.Bipolar: Has only 2 processes coming of the soma, but the dendritic process can be complex. One base connection.

As you can see, there are a variety of morphologies. However, they all have the same functional regions:

The dendrites and soma: This is where the neuron receives its inputThe Axon hillock and Axon: These allow the neuron to conduct nerve impulsesThe Axon Terminals: These are the sites of neurotransmitter release

Axon

AxonTerminals

Soma

Dendrites







Detailed Diagram of a neuron

Functions of Neurons - In order for us to understand the functions of neurons, we need to first look at the proteins that are found in the membrane, because these proteins determine the function of neurons.

Passive or leakage ion channels: These are the routes for ions to move across the membrane. They are always open and are distributed throughout the whole neuron. The channel is made up of 5 alpha helices. There are nonpolar parts (exterior) and the and polar parts (interior), causing a polar route through the nonpolar lipid bilayer that is water-filled. These leakage channels are EVERYWHERE in the neuron, but their densities are not the same everywhere.Sodium-potassium pump (Na-K pump): This pump pumps 3 Na+ ions out for every 2 K+ ions that it lets in.V-gated ion channels: These channels can be open or closed. The factor that determines whether it is open or closed is the membrane voltage. If it is more positive interiorly, this can cause the channels to open. There are 2 classes that we will be talking about mainly: Na+ and K+ channels. These occur in the axon and define the axon. Because of these channels, the axon can create and transmit nerve impulses. Ligand-gated channel: A ligand is a typically small molecule that is bound by a larger molecule - in this case, the channel protein. A ligand-gated channel is one that opens when it binds a specific ligand. Neurotransmitters are the class of ligands that we will be dealing with. These channels

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http://www.interactive-biology.com/164/biovid-episode-2-an-introduction-to-neurons/

http://www.interactive-biology.com/164/biovid-episode-2-an-introduction-to-neurons/





define, and are distributed in, the input region of the neuron (dendrites and soma). These various proteins are targeted as they are synthesized for the various regions of the neurons.

Lets take another look at the functional regions of neurons in references to the proteins:

The dendrites and soma: This is where the neuron receives its input and is the integration area of the neuron. Proteins: Ligand-gated ion channels, passive ion channels, Na-K pump.The Axon hillock and Axon: These allow the neuron to produce and conduct nerve impulses. Proteins: V-gated ion channels, passive ion channels and Na-K pump.The Axon Terminals: These are the sites of neurotransmitter (NT) release. Proteins: V-gated channels (Ca2+), passive ion channels and Na-K pump.

Ion ChannelsThe cell membrane is made up of a phospholipid bilayer and is an impenetrable barrier for ions. Cells exhibit selective permeability.

Ions can only cross cell membranes through watery pores called ion channels.If a cell has channels for a particular ion, the cell is permeable to that particular ion.Excitable cells are very permeable to K+ and slightly permeable to NA+. There are more K+ leakage channels than Na+ leakage channels

Leakage Channels are ion selective.Ion selectivity - tetrodotoxin (TTX). This is a protein that is toxic and is found in a species of japanese fish. It plugs the opening of leakage and V-gated Na+ channels, showing that they are selective for NA+.There is another toxic substance called tetraethyl ammonium (TEA), which plugs up K+ channels. More evidence that these channels are ion selective.

The inside of the membrane is negatively charged. This is due to:Negatively charged proteins that are found inside the cell.The Na-K pump, which pumps 3 Na+ out of and 2 K+ into the cell.

When you add more channels, conductance will increase and resistance decreases. If you add K+ channels the conductance of K+ will increase. If you add Na+ channels, conductance for Na+ increases. Adding K+ channels will not change conductance for Na. Conductance for K+ is 100 times greater than Na+ (passively).

There are 2 factors that control the passive movement of ions across the membrane:DiffusionCharge

Because inside the cell is negatively charged, that will pull K+ into the cell. However, Diffusion pulls it outside of the cell. This causes an equilibrium to be established when the rate of movement by diffusion equals the rate of movement by charge. This is called the Donnan Equilibrium.

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Passive ion channels and Na-K pumps are found all throughout the membranes of neurons.

Electric current is the movement of charge.



http://www.interactive-biology.com/882/ion-channels-the-proteins-in-the-membrane-of-neurons/

http://www.interactive-biology.com/882/ion-channels-the-proteins-in-the-membrane-of-neurons/





Donnan Equilibrium

The Isoelectric point of a protein is the pH at which it has a net charge of zero. If there are a lot of carboxyl groups, the isoelectric point will be more acidic. Intracellular proteins in most cells have an average isoelectric point of 4.5 - 4.7. Cellular pH is 7.2. This gives the proteins in a cell a negative charge.

Membrane potential (Em) = charge across the membrane.Resting potential (Erest) = membrane potential of a resting nerve cell.In resting neurons the membrane potential ranges between -50-80mV

Lets look at how the Donnan equilibrium is established. Lets say that we are starting off with + charged ions outside the cell. There is an electrical charge inward (due to the negative charge inside the cell), and a movement by concentration inward. The internal concentration increases. There will come a point where the concentration inside and outside will be equal. However, there will still be an inward movement due to charge.

Eventually, the concentration of that ion will be greater on the inside than outside. At this point, diffusion will then send the ion out. The charge inside is becoming less negative. There will come a point where the outward movement by concentration gradient equals the inward movement by concentration. This point is the Donnan equilibrium for that particular ion.

How to calculate Equilibrium PotentialThere are two types of work in this situation: Work done by diffusion and work done by charge attraction. At Donnan equilibrium Work by diffusion (osmotic work - OW) = work by charge attraction (Electrical work - EW). So the net work = 0

OW = RT* ln(C1/C2) EW= nFEn = charge of IonF = Farraday constantE = Voltage difference(V): E= (RT/nF)ln(C1/C2)(mV): E = 58 log(C1/C2) <--- Take home message

For a “+” charged ion: C1 = Outside concentration, and C2 = inside concentrationFor a “-” charged ion: C1= Inside concentration, and C2 = outside concentrationE = equilibrium pot. Eion = equilibrium potential for a particular ion (ENa/EK etc.)

Em (membrane potential) = -60mVConcentration ratio (10 out/1 in)Ena = 58 log (C1/C2) = 58mV

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http://www.interactive-biology.com/956/donnan-equilibrium-and-driving-force/








The Na-K pump

The Na-K pump traverses the membrane and has binding sites for both Na and K. It starts off with the pump protein in it's low energy configuration. It has an ATP bound to it but the ATP hasn't given away its phosphate as yet. The pump is open to the inside of the cell. There are 3 binding sites for Na+. When 3 Na+ bind, there is a signal that causes an inorganic phosphate (Pi) from the ATP to be transferred to the Protein. This then causes a conformational change to it's high energy state. In this high energy configuration, the pump is open to the outside of the cell. The Na no longer fits it's binding sites so Na is released.

The binding sites for K now fit K ions. When 2 K+’s binds to the binding site, then the Phosphate is removed (the ester link is hydrolyzed). ATP then attaches to the protein and the pump opens to the inside. Binding sites for K no longer fit so the 2 K+ are released to the inside.

If you get rid of all the K outside, Na will not be pumped and vice versa. Both are needed for the function of the Na-K pump.

Membrane potential of a "resting" neuronResting potential (Erest) = Membrane potential of a "resting" neuron.

Nerve impulseForce for changing Em--> nerve impulseDF = Em - EionDFna = Em - Ena = -65mV - 58mVDFna = -123mVDFk = -65mV - (-93mV) = 25mVDuring a nerve impulse:

Eion doesn't (really) changeEm does change

What has to happen before the DF can move ions?The conductance of that membrane for the ion has to increase. Something has to make that ion more able to move across the membrane. That something has to do with the V-gated ion channels. During a nerve impulse ions move across the membrane so readily that the pump is not really a factor. The conductance is really big and the ions can move quite freely across the membrane. Lets look at how that happens.

This means that the Em is far away from Ena. This will result in a force trying to move Na+ into the cell because Na+ wants to be at its equilibrium. It’s where the ion is most “comfortable”. Force to move ions across membranes = Em - Eion = Driving force (DF). So DF for Na+ will be -118mV. If the channels are opened, Na+ will rush into the cell until DF = 0 at 58 mV (all or nothing).







V-gated ion channels

Na-channel: This protein is an integral protein in the membrane. It’s presence makes the membrane axonal (in other words, it gives it the ability to produce an action potential). It traverses the membrane via 24 helices. There are 4 groups of 6 helices (alpha component). There are two features of each of these groups that we are crucial:

Helix four in each group (M4) has a bunch of amino acid residues that bear + charges (a lot of amine bearing R groups). This is the trigger that opens the v-gated Na Channels. It is a positively charge voltage sensor. There are at least 40 different genes that encode for V-gated Na channels and there are variants on a theme. When we talk about the v-gated Na channel we are generalizing. Between M5 and M6, there is a loop of amino acids that is not in helix formation. These loops lines the pore providing the environment that the Na ions move through. These are also what makes the channel selective.

Subcomponents of the V-Gated Na ChannelSelectivity filter - involves critically located negative charges (CO-OH R groups) and residues that remove the hydration shell from Na ions.Activation gate - It is a piece of the protein that can close and open the pore. It is a sequence of amino acids that face the inside of the membrane. Voltage sensor: positively charged helix pore. Helix 4- repelled outward by a positive change in Em. The positive helices are repelled towards the outside of the cell when there is a positive change on the inside of the cell (positive repels positive). It is linked to the activation gate and causes it to open. Na ions can then move in. The opening of this channel can only be described in terms of probability. There isn't a particular value that all of them will open at. Some channels require a bigger positive change.

There is also an inactivation gate that closes automatically about .5 -1ms. This channel cannot be opened again until the Em inside gets back negative when the nerve impulse is nearly over.

The Voltage gated K channel has no inactivation gate and stays open longer than the V-gated Na channel. The amount of positive change that makes K gate open is much greater than that for Na channels. That means that Na channels open first.

Conductance

Gna is the conductance of the axonal membrane for Na. Erest = -70. Ek=-93. Ena=58. If conductance of the membrane goes up for Na it's going to move in. Ethres: firing threshold for the neuron.

Definition of threshold: The threshold is the membrane potential that when reached will result in a nerve impulse.

It is crucial that the v-gated Na channels open at a lower membrane potential than K channels, because the membrane potential wouldn't change much. As Na comes in, K would go out.







Because Em reaches a value where increase in Gna that is significantly greater than the increase of Gk, this results in more Na entering than K leaving, thus the Em becomes more positive. If Em becomes more positive, Gna will increase. More v-gated Na channels will open, and Em becomes more positive (positive feedback).

Definition of Threshold revisited: Threshold is the membrane potential that results in a greater increase in Gna than in Gk. The threshold varies depending on the architecture of the axon, especially in the spike initiating zone.

In the situation when the resting potential reaches the threshold we get the positive feedback, which results in a nerve impulse (action potential).







The Nerve Impulse/Action Potential

Here are the Sequence of events that will lead to the production of a nerve impulse/action potential:

A stimulus causes Em to reach the threshold. This means that more v-gated Na channels open than v-gated K channels, which also means that more Na enters than K leaves (large DFna). Therefore, Em becomes more "+".As Em becomes more positive, more v-gated Na channels open, which means that Gna increases, which means more Na enters. This is called depolarization.Essentially all v-gated Na channels open and Gna becomes maximal. Therefore Em approaches Ena. The driving force for Na decreases and inactivation gates start closing. At this point, V-gated K channels start to open. Nerve impulses reaches a peak near Ena. During repolarization. V-gated Na channels inactivate, V-gated K channels open, membrane potential moves towards Ek (negative).After hyperpolarization. Em->Ek. V-gated K channels are closing. V-gated Na channels reset to close.

Repolarization is necessary to reset the v-gated Na channels from inactivated to their closed conformation.

Refractory PeriodsWhenever an action potential happens in a neuron, there is a period that follows wherein it is difficult to cause another action potential. This is called the refractory period. There are two types:

Absolute refractory period: During this period, the axon cannot be stimulated strongly enough to create another action potential. The firing threshold is infinitely high. No matter how strongly you stimulate the axon during this period, no impulse will happen. This is because it is a period during which V-gated Na channels are either open or inactive. In these states, they cannot be “reopened”. V-gated Na channels start resetting at the end of the absolute refractory period.Relative refractory period: It takes a higher than normal (resting) stimulus to create an action potential.

Early in the relative refractory period, the threshold is very high, which means that it takes a very large stimulus to create an action potential because only a few v-gated Na channels are reset to closed.In the middle of the relative refractory period, the threshold is higher than during rest but lower than at the beginning. This requires a stimulus that is larger than rest but smaller than at the beginning. This is because more v-gated Na channels are reset to closed.

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http://www.interactive-biology.com/1541/what-is-an-action-potential-episode-7/

http://www.interactive-biology.com/1541/what-is-an-action-potential-episode-7/

http://www.interactive-biology.com/1572/depolarization-phase-1-of-the-action-potential-episode-9/

http://www.interactive-biology.com/1572/depolarization-phase-1-of-the-action-potential-episode-9/

http://www.interactive-biology.com/1579/repolarization-phase-2-of-the-action-potential-episode-10/

http://www.interactive-biology.com/1579/repolarization-phase-2-of-the-action-potential-episode-10/

http://www.interactive-biology.com/1584/hyperpolarization-last-phase-of-the-action-potential-episode-11/

http://www.interactive-biology.com/1584/hyperpolarization-last-phase-of-the-action-potential-episode-11/





At the end of the relative refractory period, threshold reaches its lowest value, which is typical of rest. The stimulus required for threshold equals what is required at rest. All v-gated channels are closed.

Conduction VelocityWhen an action potential begins, Na enters into the cell and positive charges are repelled in both direction. This is electrical conduction along the axon and is called electrotonic conduction. This current is made up of positive charges. It is fast and progressively lost (due to resistance). The movement of the Na across the membrane is not nearly as fast as current flow along the membrane, but is not lost, because it is determined by Ena. So Electrotonic conduction is faster than movement across the membrane. Eventually, the current that flows along the axon will die out, or will be too small to reach firing threshold, and have to wait for the slower process of moving Na across the membrane to catch up.

The larger λ is, the faster the conduction velocity will be. Large diameter axons conduct nerve impulses faster because they conserve that longitudinal electrical current due to the lower Longitudinal resistance.The axons in most nerves are myelenated. This means that in the peripheral nervous system (PNS), Schwann cells envelop the axon and grow around the axon so that we end up with a number of layers. The Schwann cells are full of myelin, which is a non conducting lipid material. The Schwann cell envelops the axon with an impenetrable barrier for ions. This makes Rm much much greater, and the nerve impulse will travel much faster.

There are no v-gated channels under the Schwann cell. They are only found at the nodes. This also allows the action potential to travel faster because it doesn’t have to wait for v-gated Na channels to open all along the axon, which is a slower process. It “jumps” from node to node in a process called saltatory conduction.

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λ = √(rm/rl)

rm: Resistance across the membrane of the axonrl: Resistance along the length of the axon

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In a nerve, there are many axons. There’s a fast conducting group (alphas), a bit slower group (betas) and a slow group (gammas), so when you look at the electrical activity of the nerve in a graph, you will often see 3 peaks.



http://www.interactive-biology.com/1591/the-absolute-and-relative-refractory-periods-episode-12/

http://www.interactive-biology.com/1591/the-absolute-and-relative-refractory-periods-episode-12/

http://www.interactive-biology.com/1609/saltatory-conduction-episode-15/

http://www.interactive-biology.com/1609/saltatory-conduction-episode-15/





THE SYNAPSEElectrical conductionWhen the signal is going to flow from one neuron to the next, it encounters resistance. The resistance of the presynaptic membrane is approximately 1011 ohm. The resistance is the synaptic cleft is 108 ohm. The post synaptic resistance is 1011 ohm. The current will go to the environment with least resistance, so most of the current will be lost via the smaller resistance in the synaptic cleft.

One way of decreasing the resistance is by having a large presynaptic membrane (lower resistance of 105 ohm), a small synaptic cleft (higher resistance of 1011 ohm) and and having a large postsynaptic membrane. With this setup, the current will go to the postsynaptic membrane with the smaller resistance instead of leaving the synaptic cleft with a big resistance.

There are gap junctions in the pre and post synaptic membrane. A gap junction is an array of 2 sets of connexons with direct electrical access from 1 cell to the next. Some connexons can be either open or closed.

Axon terminals (telodendrites) - Release neurotransmittersThe synaptic bouton is characterized by being filled with synaptic vesicles. They contain neurotransmitter. There is a special postsynaptic membrane that responds to the neurotransmitter molecules from the presynaptic membrane.

In the synaptic bouton, we find Ca pumps taking Ca out, and v-gated Ca channels that brings Ca in. When a nerve impulse comes along, V-gated Ca channels open and Ca moves into the bouton, and that starts the process to release neurotransmitter into the synaptic cleft.

Starting conditions We have synaptic vesicles in the terminal. They are inactive.

Synaptic vesicles are anchored to actin filaments by the protein synapsin I. As nerve impulse comes along, V- gated Ca channels open and Ca goes inside the terminals. First, 4 Ca ions are picked up by an internal protein called calmodulin, which then makes it active. Calmodulin then activates a calmodulin-dependant protein kinase (protein kinase II). Protein Kinase II causes synapsin to release the synaptic vesicle from the actin fiber. Now we go into the docking stage.

There are two other proteins on the synaptic vesicle called synaptophysin and synaptobrevin that are involved in the docking process. Ca binds to these 2 proteins and activates them, causing them to separate.

Synaptobrevin acts as a V-SNARE. There are 2 proteins in the presynaptic membrane that determines where docking will take place, SNAP-25 and syntaxin (makes a T-SNARE). The combination of V-SNARE and T-SNARE allows for the docking of the synaptic vesicle to the presynaptic membrane.

Kinases are enzymes that catalyses phophorylation of proteins. The most likely parts of a protein to be phosphorylated is an R group with an OH







There is another protein called synaptotagmin (located on the vesicle), that leads to the fusion with the presynaptic membrane. This causes exocytosis of neurotransmitter into the synaptic cleft.

The fusion of the membranes causes to bouton to increase in size. And because of this, you get a recycling process in which you get new synaptic vesicles breaking off at the neck. The NT goes across the synaptic cleft and binds to receptors in the dendritic membrane and open ion channels.

The Chemical synapse - post synapticTwo types of Receptors (for neurotransmitters):

Ionotropic receptor - These are fast acting receptors. The neurotransmitter binds to the receptor site on the protein and the protein includes a ion selective channel which opens as a result of binding (ligand-gated ion channels)Metabotropic receptor - Neurotransmitter binds to a protein receptor in the membrane which goes to the activation of a G-protein which usually activates a second messenger system.

Examples of post synaptic receptors:The Nicotinic receptorThis receptor binds the neurotransmitter acetylcholine (ACh). When ACh binds to the receptor, it opens the channel and the predominant effect is that Na+ moves into the cell. K+ also leaves, but the overwhelming effect is Na+ coming in due to its strong driving force.

The nicotinic receptor is made up of 5 subunits. There are 2 alpha subunits. It takes 2 ACh's to bind the 2 alpha subunits to open the channel. When the ACh binds to the 2 separate alpha units, the channel

Watch Video

Nicotine also activates the nicotinic receptor, and thats why we call nicotine an agonist (a molecule that mimics the effect of NT). Chemicals that have effects on the Nervous system (psychotropic) affect the behavior of NT.



http://www.interactive-biology.com/1617/the-release-of-neurotransmitter-episode-16-2/

http://www.interactive-biology.com/1617/the-release-of-neurotransmitter-episode-16-2/





opens and the net effect is Na entering. When Na enters we get an excitatory post synaptic potential (EPSP).

The ACh is then quickly released so the channels can close. There is also an enzyme called acetylcholinesterase that brakes down acetylcholine and inactivates it.

When a neurotransmitter binds to a ionotropic receptor, the result is either a depolarizing or hyperpolarizing change in dendritic Em. If it depolarizes we call it an EPSP. If it hyperpolarizes (inhibits) we call it an IPSP.

Synaptic transfer: What happens between the dendrite and axon. When Na+ enters, this will change the membrane potential and makes the inside more positive EPSP. This positive charge flows by electrotonic conduction down to the Spike initiating zone. If it is large enough to make it to threshold, it causes the production of a nerve impulse.

When a nerve impulse is created, you cannot make another one. There will be a period of time when the threshold is infinitely high. This is the absolute refractory period (ARP). Big EPSP make nerve impulses faster than small EPSP because the firing threshold during RRP drops below the membrane potential of the EPSP sooner. This means that more NT can make even bigger EPSP's that makes more nerve impulses even quicker.

There is an opposite kind of response in ionotropic receptors of different types.Inhibition - for inhibition we need a different neurotransmitter and we need a different ionotropic receptor. There are two important NT's - GABA and glycine. These both affect two different receptors, but both open and close Cl- channel. There has to be a Cl pump that pumps Cl-. GABA is the most common.

The DF for Cl moves it in and we get an IPSP. This will travel electrotonically down on to the axon as well. This will only be meaningful in that it can stop a nerve impulse from being created.There are 2 common poisons that affect inhibitory ionotropic receptors: strychnine and arsenic. Strychnine is an inhibitor/antagonist for the ionotropic receptor that responds to glycine. It will eliminate IPSP's and Nerve impulses will travel like CRAZY.

Summation and facilitation

Summation is the addition of PSPs. There are two types of summation:Spatial Summation - summating PSPs originate from 2 different synaptic inputs.Temporal Summation - summating PSPs originate from the same synaptic input.

There is a very crucial factor --> Summation requires a time overlap, whether we are talking about temporal or spatial summation.

Watch Video

The control by the central nervous system is like having a whole series of traffic stops at each synapse. It is the pathway control by the CNS that controls your behavior.



http://www.interactive-biology.com/1641/agonists-and-antagonists-episode-18/

http://www.interactive-biology.com/1641/agonists-and-antagonists-episode-18/





Facilitation is a process that results in increased NT release as a result of a presynaptic synapse, activating a second messenger system. Sensory neuron responds to stimulus, releases NT and creates a response in Motor neuron that we are recording. An axon terminal releases NT to the Presynaptic membrane. The NT is seratonin.

A seratonin receptor binds seratonin (metabotropic) from the facilitory neuron. This activates a G-protein, which activates an adenylate cyclase, which produces cAMP (2nd messenger). This cAMP activates a cAMP-dependent protein kinase (pk). This phosphorylates a K channel in the bouton. This K channel closes. Repolarization slows down so nerve impulse lasts longer, and more v-gated Ca channels stay open longer. More Ca gets in, more vesicles fuse with the membrane, thus more NT released.

The degree of facilitation changes depending on how much time is elapsed between the initial and subsequent response.

The Muscarinic receptor - A metabotropic receptor for acetylcholine is the muscarinic receptor, so called because muscarine is the agonist (artificial anologue). It has 7 transmembrane helices and between helix 3 and 4, there is a binding site for ACh. There is also a signal loop that contacts the G protein, breaking it down in such a way that the G protein attaches to the channel and closes it.**There are a variety of different ways that acetylcholine can affect different muscarinic receptors.**

All of the small NT that are involved with ionotropic receptors also have metabotropic receptors that respond to them. The role of a metabotropic receptor is to regulate some process, not to directly produce PSPs like ionotropic receptors.

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http://www.interactive-biology.com/1660/what-is-summation-2-types-%E2%80%93-episode-19/

http://www.interactive-biology.com/1660/what-is-summation-2-types-%E2%80%93-episode-19/

http://www.interactive-biology.com/1666/facilitation-episode-20/

http://www.interactive-biology.com/1666/facilitation-episode-20/





Neurotransmitters, agonists and antagonists

Fast - ionotropic: NT is always a "small" molecule. Examples are ACh and Glutamate (both excitatory), GABA and Glycine (inhibitory), Dopamine and seratonin (some cases). In the fast neurotransmitter system, ACh and glutamate will be consistently excitatory, and GABA and glycine are consistently inhibitory. In the slow system they can be either fast or slow.

Slow - metabotropic.

Cholinergic - ACh-likeAChSuccinyl choline (agonist)

CarbabholNicotine (it's presence multiplies the effect of ACh). This causes the nervous system to slow down the release of ACh. Then you become dependent of that substance to return back to normal --> General mechanism of addiction.Curare: Antagonist for ACH. It blocks the channel in nicotinic receptors by attaching to the binding site, paralyzing the muscle.

Monoamines Adrenergic (has affects similar to adrenaline/epinephrine)Catacholamine. Dopamine is the "feel good" molecule in the nervous system. It is produced by dopaminergic neurons. When these neurons die, it results in Parkinson's disease. Injecting dope was one of the first ways of treating Parkinson’s.Cocaine has it's major effect by increasing dopamine levels by slowing down the inactivation of dopamine. Then you get the same addictive effect. Which NT is released is a function of how far the pathway goes. Mescaline has an effect that mimics dopamine (sort of an agonist). Speed increases the production of Epinephrine and norepinephrine tremendously. Seratonin is another "feel-good" molecule. It is very intimately related to your sense of well-being. This is related to depression. An individual with low levels is more likely to become depressed. Prozac raises seratonin levels by slowing down the inactivation of seratonin.

Amino Acid NeurotransmittersGlutamic acid - most important excitatory NT. It is a CNS NT in vertebrates. It is secreted within neurons, put into synaptic vesicles and is secreted at synapses.Glycine and GABA - inhibitory. The only difference between GABA and Glutamate is 1 COOH group. The GABA receptor includes a ligand gated Cl- channel. The GABA channel has some modulatory sites. The substances that modulates this channel are called modulators (not agonists). On the GABA receptor there is a benzodiazapine site.

Valium is a common benzodiazapine. Valium is a tranquilizers/anxiolitic substance. Xanax is also a benzodiazapine. When a bazodiazapine attaches to the site and then GABA attaches, the channel opens and stays open longer. Without a benzodiazapine, the channel does not open as long. So benzodiazapines increase inhibition and are used to help you sleep. Barbituates operate in the same way but are more addictive.

Neuropeptides - released in large vesicles.Opioids - creates a sense of euphoria and blocks pain - endorphins/enkepalins. They are normally produced. Endorphins seems to be produced as a result of physical excercise. They block pain pathways.Substance P - one of it's effects is to increase the input of pain inducing stimuli.







Organization of the Nervous System

It is estimated that there are over 100 billion neurons in the human body. Needless to say, there is need for a significant amount of organization within the nervous system.The Nervous system is divided into 2 Parts:

The Central Nervous System (CNS): this is made up of the brain and spinal cord. This is where the control happens.The Peripheral Nervous System (PNS): this is everything outside of the CNS (i.e. nerves). The main purpose of the PNS is to connect the CNS to the limbs and organs.

Groups of NeuronsThere are clusters of neurons found throughout the nervous system. If these structures are found within the CNS, they are refered to as nuclei (singular: nucleus). If they are found outside the CNS, they are refered to as ganglia (singular: ganglion).

Organization of the spinal cordIn the spinal cord we have

Gray matter, which is on the inside - This is where we find all the synaptic connections and somata. It is where control happensWhite matter, which is on the outside - It contains myelenated axons and is the “wiring” of the system.

The white matter is divided into tracts/pathways. These tracts contains axons that are going to similar parts of the nervous system. If there is damage in the reflex, that suggest that there is damage with the corresponding tract. That is why doctors take reflex tests.

ReflexesSome of the most elemental processes happens at the spinal cord in a predictable way. The Knee jerk reflex is extremely simple because the sensory neuron connects directly to a motor neuron and the response is uncontrollable. Because there is no place for further processing to occur, if there is a stimulus, there WILL BE a response. As interneurons are placed in the center, it becomes more sophisticated.

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http://www.interactive-biology.com/2679/063-the-divisions-of-the-nervous-system/

http://www.interactive-biology.com/2679/063-the-divisions-of-the-nervous-system/

http://www.interactive-biology.com/1698/how-reflexes-work-knee-jerk-and-eye-blink-episode-23/

http://www.interactive-biology.com/1698/how-reflexes-work-knee-jerk-and-eye-blink-episode-23/





There is a single interneuron in the eye jerk reflex so it is controllable (if you try really hard). This type of setup is refered to as a simple reflex arc, where there is a sensory neuron that transfers the signal to an interneuron (relay neuron) in the spinal cord, which then transfers a signal to a motor neuron, which goes to the muscle. Where the axons come together in a bundle we call a nerve. The nerve splits into a dorsal root (sensory) and a ventral root (motor) when it is entering the spinal cord. The morphology of sensory neurons is typically pseudounipolar running from body receptors running to the spinal cord.

There are pain receptors in the finger. Lets say that you touch a hot stove. Sensory neurons are stimulated and send a signal to the spinal cord. This causes a reflex that is mediated by the spinal cord. This causes the jerk reflex. However, there is also synaptic transfer that goes all the way up via the spinal cord and to the somasetic cortex and that is where feeling comes into play.

Different touch receptors in the body make different connections but they all end in the somasetic cortex. This part in the brain does not send anything back to the region of pain. The pain is actually “in your mind”.

The connection of the body to the brain also happens on the motor side, so movement or the motor response is done by the motor cortex in the brain.







Organization of the brainThe brain starts where the spinal cord enters the occipital bone through the foramen magnum (opening of the skull). There is no sudden change in the organization once the spinal cord enters the foramen magnum. No anatomical difference exists between just inside the brain and just outside the brain.

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The Brain Stem: This is the Lower part of the brain and includes the following

The medulla. It is relatively simple in organization, not very big but crucially important. It is involved in the regulation of many of the bodily processes that are controlled automatically like blood pressure, heart rate, respiration etc (autonomic functions). The Pons. This is located directly above the medulla and regulates relaxation The Midbrain.

Cerebellum - dorsal outgrowth of the medulla. It is involved in the control of movement. Resent research indicates that it is also involved in spatially organized senses and movement, and even spatial memory. To move an object from one place to the next, you always base movement on the knowledge of movement just accomplished.

The cerebellum is checking the command to move with the movement accomplished. If the two don’t match it corrects it. There is feedback to the cerebellum of movement and error correction is dependent on the cerebellum. One of the most obvious results of damage in this region is spastic. This is a loss of coordination.

Thalamus + hypothalamus: These are outgrowths of a region of the developing brain called the diencephalons (developmental term). They are not huge but extremely important.

The hypothalamus has a number of important functions. The posterior pituitary is a direct outgrowth of the hypothalamus. The posterior pituitary combined with the anterior pituitary make up the pituitary gland. The anterior pituitary does not develop from the brain, but is controlled by the brain in a very heavy way. It controls much of the rest of the endocrine system and it is in turn controlled by hypothalamic neurons. In the hypothalamus, there are a number of regions involved in control of behavior and other physiological processes. e.g. we can identify specific groups of neurons in the hypothalamus, destroy them and the experimental animal will eat itself to death in about a week. There are neurons, which produce neurochemicals that says "That is enough already", which turns down the sense of hunger.

There are other nerve cells that do the opposite. They produce neurochemicals that stimulate

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http://www.interactive-biology.com/1835/the-3-parts-of-the-brain-stem-and-their-functions-%E2%80%93-episode-27/

http://www.interactive-biology.com/1835/the-3-parts-of-the-brain-stem-and-their-functions-%E2%80%93-episode-27/

http://www.interactive-biology.com/1830/the-function-of-the-cerebellum-%E2%80%93-episode-26/

http://www.interactive-biology.com/1830/the-function-of-the-cerebellum-%E2%80%93-episode-26/





hunger. If they are missing, the experimental organisms will starve to death. There are other neurons that if you inject concentrated salt solution, the animal starts drinking. These nerve cells detect the osmolarity of the cerebral fluid and tell the animal to drink. This shows only a few of the physiological and behavioral processes controlled by the hypothalamus. The hypothalamus controls the cerebral hemisphere.The Thalamus: These are the walls of the tube. It is just above the hypothalamus and regulates, in very important ways, the functioning of the cerebral cortex. Nerve traffic in and out of the cerebral cortex to the rest of the body all goes through the thalamus. If you are going to move, that's a result of what happens in your cortex, but the command neurons for your moving makes synaptic connections in the thalamus before going to the rest of the body. It is a “regulatory gateway” to the rest of the body.

There are two Cerebral Hemispheres. In the spinal cord, gray matter is central, and white matter surrounds it. In the cerebral hemispheres most of the gray matter is on the surface. We use the term cerebral cortex to refer to the outer surface of the cerebral hemispheres. It is typically only 8-10 layers deep. The blood supply comes from the surface. This is clearly the most metabolically active part of the brain.

The central white matter (myelenated axons) gives you the bulk of the cerebral hemispheres. The corpus callosum, along with some other connections, connects the 2 hemispheres and coordinates what happens between the left and right hemispheres.

The Cerebral cortexThe visual association area is a region that is very active when you are building complex visual images. The general interpretive area is active in putting together different types of stimuli (e.g. smell and vision. The visual cortex is primary. The general interpretive area is more complex. The motor cortex is just anterior to the central sulcus.

The most anterior part of the motor cortex controls the most posterior part of the body. The right motor cortex controls the left side of the body and vice versa. Your body is represented upside down and backwards in the brain. Right=Left and Up=down.

The degree of control puts a requirement on the nervous system puts a demand for more neurons. The more finely we control movement, the more of the motor cortex we take up. A big part of the motor cortex is for speech.

You can't teach a monkey to speak because they have a smaller portion of the motor cortex attributed to speech. However, these animals are more highly coordinated muscularly than we are, so they can be taught to speak sign language.

The way station in vision is the lateral geniculate. This is a region of the thalamus. The thalamus is also a gateway for regulating consciousness.

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http://www.interactive-biology.com/1839/the-thalamus-and-hypothalamus-%E2%80%93-episode-28/

http://www.interactive-biology.com/1839/the-thalamus-and-hypothalamus-%E2%80%93-episode-28/





The motor association area is next to the motor cortex and is crucial to developing finely tuned movements. The primary motor cortex will send the signals out, but it will go through the motor association area.

The broca's area is associated to speech. Damage to this area will result in organisms that cannot form words.

Somasthetic cortexSensory area (cortex)Somatic association area - where more highly developed body based sensory experiences are located. This is where your body position sense is put together.

Intellectual functionsYour intellectual function is an outcome of everything your brain is doing. The frontal and prefrontal lobes are very important in intellectual functions. The thalamus is also very much involved. The thalamus is the interconnecter, and in intellectual function the activity of different parts of the cortex are interconnected through the thalamus. Another important part are the association areas. They integrate input from different senses to make complex integrations of what's going on.

One of the most important functions of intellectual functions is MEMORY - By memory we mean the ability to be aware of something that has happened and is no longer happening. Memory happens in stages:

The first stage is sensory memory: The ability to remember the information from where your eyes just was and connect it to where you eyes are now - e.g. reading - (seconds)Short term memory: (1 - 2 hours). Based in part on an "active circuit". There are pathways in your brain that get connected and reverberate. In addition there are also some molecular components. Long term memory: clearly dependent on molecular changes at different places in the cortex. There is one region of the cortex called the hippocampus. Damage to or deterioration of the hippocampus retards memory.

CONSCIOUSNESSThe hypothalamus and thalamus are involved in regulating the change from conscious to unconscious and vice versa. In the hypothalamus there are groups of neurons that seem to induce sleep/unconsciousness and other groups that seem to induce consciousness, but it does it through the thalamus.The reticular activating system (RAS) - based on a network of interconnected neurons, located primarily in the brain stem - reticular formation. It interconnects with the hypothalamic and thalamic stems. Sensory input goes to the RAS as well as to the parts of the brain where you get sensory experience. The sensory input activates the RAS. When someone pokes you in your sleep and you wake up, it is not because of the touch but it is because it goes to the RAS.

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Consolidation: Transformation of short term into long term. It happens when you sleep. Especially happens in REM (rapid eye movement) sleep. MMDA receptors are important in this process.



http://www.interactive-biology.com/1818/the-4-lobes-of-the-cerebrum-and-their-functions-episode-25/

http://www.interactive-biology.com/1818/the-4-lobes-of-the-cerebrum-and-their-functions-episode-25/





If you are awake and you are put into an area where there is hardly any sensory stimulus (sensory depravation), you begin to hallucinate and after a while you can get emotional problems. Sleep is unconsciousness. Deep sleep is marked by a delta wave in the EEG. There is hardly any brain activity. In the sleep cycle you tend to have varying levels of consciousness. It cycles. The time-period between 2 points in a cycle is typically 1.5 - 2 hrs.

The High point in the cycle is called REM sleep. Here is when you dream. Everyone should dream every 1.5-2 hours. This is also where consolidation happens. It is called Rapid eye movement sleep because if you put electrodes in the corner of the eye you will see muscle contractions in the eye.

Sleep rhythm is very important, and if you don’t have enough alpha and delta waves, you can go crazy.







THE SENSORY NERVOUS SYSTEM

ReceptorsThere are two types of receptor cells from a developmental perspective:

Primary - neuron or derived from neuron. Developmentally, they are derived from the neuroblast - embryonic cells that produce a number of different kind of cells, one of which are neurons. Secondary - Epidermal derivative but not from Neuroblast. (comes from the part of epiderm that makes the body covering). The receptors respond to stimuli and usually cause in the increase of neurotransmitter release.

Common mechanism - production of a change in membrane potential, which is excitatory - Receptor potential (generator potential). Receptor cells are specialized to respond to a particular class of stimulation.

Pacinian corpuscle - has a special series of membranes surrounding the ending of a neuron (where a dendrite would be). It responds to applied pressure by depolarizing (receptor potential). As stimulus strength increases, we see that Em change increases. If it reaches threshold, you get an action potential. receptor potentials either produce AP's directly or cause the release of neurotransmitter, and the NT produces AP's in another cell. Receptor potential acts as an EPSP.

Mechanoreceptors - based on the stimulus stretching it open. The more of these channels open, the bigger the Receptor potential. Strong stimuli produce a bigger receptor potentials. Bigger receptor potentials makes faster nerve impulses (more frequently).

Stretch receptors (e.g. crayfish) - located along the muscle. Stretching moves these dendrites, located in these dendrites are the same kind of channels as in the mechanoreceptors. If the stretch is small we see a small receptor potential --> slow nerve impulses. If the stretch is large we see a large receptor potential and that will lead to quicker nerve impulses.

Tonic stretch receptor - Continually "fires" in response to an unchanging stimulus.Phasic receptor - completely adapts to an unchanging stimulus. They respond specifically to change in stimulus.

Receptors without axons (no APs produced by receptor). The stimulus strikes the receptor, and the receptor responds with a receptor potential and there is an increase in the release of NT, which then goes to an EPSP postsynaptically and then action potentials in a sensory neuron.

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http://www.interactive-biology.com/1844/a-general-overview-of-how-senses-work-%E2%80%93-episode-29/

http://www.interactive-biology.com/1844/a-general-overview-of-how-senses-work-%E2%80%93-episode-29/





Photoreception

Different color light have different wavelengths. When light moves, it is moving in a linear direction while oscillating. Wavelength is the length of one full oscillation. Photons are a kind of electromagnetic radiation.

Can photons that have the same wavelength transfer different amounts of energy? Not usually. Bright and dim is a function of the amount of photons.

The energy associated with a photon is called the quantum. Shorter wavelengths have more energy. E.g. UV light is damaging because of the large amount of energy.

The camera eyeAccommodation (focusing).Control of the amount of light which goes to the retina (pupil).Image formation on the retina.Receptors - Rods and cones

General overview of visionLight enters the eyes through the pupil. The pupil determines how much light enters. The lens then focuses the light onto the retina, where the rods and cones are.

The rods and cones transfer signals to the bipolar cells, which then transfers the signal to ganglion cells - the cells that make up the optic nerve.

The ganglion cells project (sends a connection to) to the lateral geniculate (structure in the thalamus). All of the optic fibers end in the lateral geniculate.

Interneuron - a neuron that is wholly contained within the CNS. The lateral geniculate fibers that project to the visual cortex are interneurons. The vision occurs in a region of the midbrain called the optic tectum in amphibians.

The Nitty Gritty of vision

Lets take a look at what happens inside the rods when light hits the retina. The process that happens in the cones are relatively similar to what happens in the rods.

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http://www.interactive-biology.com/1849/how-eyes-work-%E2%80%93-an-introduction-%E2%80%93-episode-30/








Rhodopsin is the visual pigment that is found in the outer segment of rods. Rhodopsin has two subunits, a small molecule called retinal (slightly processed vitamin A), and a big protein called Opsin. Retinol has 2 states, a cis state and a trans state. The cis state is a higher energy configuration. Retinol in rhodopsin is called cis retinol. The numbers is the maximum wavelength of absorption.

When a photon strikes a rhodopsin molecule, the energy is used to change retinol to its low energy configuration (trans). Thats all the photon contributes to the process. The retinol then begins to break away from the opsin. This breakdown continues spontaneously until they are separated.

Opsin is an enzyme. It is inactive in its rhodopsin form. When retinol breaks away from opsin, it opens up a catalytic site (active site). In the rod there is a G protein called transducin. Opsin catalyzes the addition of a GTP to the Talpha subunit of the G protein (substitution). This removes the inactivating subunits. The Talpha GTP activates another enzyme (phosphodiesterase) which breaks down cAMP or cGMP. This phosphodiesterase is inactive because of the two inactivating alpha proteins. The two alpha units are removed by the phosphodiesterase so that we free up an active cGMP phosphodiesterase. The transducin takes on the alpha subunits.

The crucial event that leads to vision is next. The phosphodiesterase breaks down cGMP, and it is this single step that leads to vision.

Talpha from transducin then activates cGMP phosphodiesterase by taking off the 2 alpha subunits (phosphodiesterases always inactivate cAMP of cGMP). This suggests that cGMP is in high concentration and that light lowers this concentration.There are two enzymes in this pathway: Opsin and Phosphodiesterase. Thus, 2 sites of amplification

In the outer segment of the rod there are Na channels that are open when cGMP is present. When cGMP is broken down, this closes these cGMP dependent Na channels, which decreases Na conductance in the outer segment. In the rod, this happens in the outer segment, meaning that in the dark a rod has a high Na conductance. Gna = (approx) Gk. This means that the resting potential will be positive. Em = (approx) (Ena+Ek)/2

In the light, Gna<Ek. Em approaches Ek. This will lead to a hyperpolarization.

Rods do not have the proteins in the membrane, nor the structure to produce nerve impulses. It does have a lot of synaptic vesicles. In the dark, Em is more positive than Erest. There is a increase of neurotransmitter release of NT. In the light, Em goes towards Ek, the result is a decrease in the release of NT.

Summary of Vision (up to this point):Photon of light enters the eye via the pupilLens focuses light onto retinaIn the Rods

Photon strikes rhodopsinRetinal changes from cis to trans formRetinal breaks away from Opsin exposing the active siteOpsin catalyzes the substitution of GTP on Talpha subunit of Transducin

THE RECEPTOR POTENTIAL CHANGE IN RESPONSE TO LIGHT IS HYPERPOLARIZED CAUSING A REDUCTION IN NT RELEASE







Talpha GTP activates phosphodiesterase (PDE)PDE breaks down cGMPThis closes cGMP-dependent Na ChannelsThe rod HYPERPOLARIZES

Amplification is really important because a single photon is enough to see light.

Retinal structure There are a few layers in the retinal structure:

The receptors - rods and conesBipolar cellsGanglion cells - somata of optic nerve fibers.Amacrine cellsHorizontal cells ---> modifying cells.

The breakdown of rhodopsin leads to hyperpolarization, which reduces NT release between the rod and bipolar cells.These cells depolarize as a result of the reduction of neurotransmitter release by the rod or cones. The hyperpolarization of the rod leads to the depolarization of the bipolar cells. Bipolar cells have no axon, so the EPSP travels electrotonically.

The ganglion cells produces nerve impulses in response to the release of NT from the bipolar cells. This is the first place we see nerve impulses. These processes lead to vision.

Organization of photoreceptorsRods - 125,000,000/retina

Rhodopsin is the pigment in Rods. Rods are more sensitive to light than cones are. 100x more sensitive than cones.Leads to black and white visionVision is not very high in detail. Rods are uncommon in the center of the retina (visual center/fovea).

Cones3 other visual pigments in the cones - red, blue and green absorbing pigments. Each of these pigments are built like rhodopsin, but the protein is somewhat different. They are activated by light in the same way. The effect on Na conductance is the same, except they don't absorb light quite as readily. These leads to color vision.There are "only" 6,000,000 cones/retinaConcentrated in the center of the retina (fovea). We use cones for detail vision

Ganglion cellsOnly 1,000,000/retina

Receptive field of a ganglion cell

Light has to go through all these cell layers to reach the pigment layer

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http://www.interactive-biology.com/1872/visual-processing-in-the-retina-%E2%80%93-episode-32/

http://www.interactive-biology.com/1872/visual-processing-in-the-retina-%E2%80%93-episode-32/





Each ganglion cell has a receptive field, which is defined by the location of the receptors that it is connected to in the retina. Receptor density also determines the ability to discriminate 2 points.There are 150,000 cones/mm2 in the fovea. That means that they are very tightly packed. A ganglion cell in this region can be connected to a single cone. That means that it's receptive field is very detailed.

As you go out to the lateral edges of the retina, density of receptors goes down and the number of receptors attached to ganglion cells goes up to sometimes thousands of receptors, mostly rods.There are cones throughout the retina, but they are relatively very low in number.

Cones come in three types. In order for the brain to interpret what is happening on the retina it would have to know what type of receptors a particular ganglion cell are where the receptive field for the ganglion cell is. This label is anatomical and the general picture is called "the principle of connectivity". It is how the sensory neurons are attached to the visual center that defines what the brain gets out of that stimulation. This principle is a general principle, not just visual. Any nerve impulse coming over a particular sensory connection will be interpreted by the brain based on the connectivity of the neurons.

Cortical maps

In an experiment the target shaped stimulus with radial lines was centered on the visual fields of a monkey. They sacrificed the animal, cut up the visual cortex and used the technique which would stain darkly the cortical neurons that were active before the cut was made. What was noticed was that the same spatial pattern was represented on the cortex of the brain.

The spatial relationship between the receptors that were stimulated is retained in the organization of response in the cortex. A cortical map is a term we apply to the fact that the spatial location of receptors that are stimulated is represented in a map-like fashion in the appropriate area in the cortex.

VISUAL PROCESSING

Visual edges are sharpened and make more contrast. When you have a lighter gray and a darker grey, the processing in the retina emphasizes the edge. If you look at Rectangles A, B and C, you will notice that Rectangle B is slightly lighter to the left. However, Rectangles B and C are identical. The edges are emphasized because it’s next to the darker rectangle. This is due to processing that happens in the retina.

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http://www.interactive-biology.com/1881/the-receptive-field-of-a-ganglion-cell-%E2%80%93-episode-33/

http://www.interactive-biology.com/1881/the-receptive-field-of-a-ganglion-cell-%E2%80%93-episode-33/

http://www.interactive-biology.com/1886/how-lateral-inhibition-enhances-visual-edges-%E2%80%93-episode-34/

http://www.interactive-biology.com/1886/how-lateral-inhibition-enhances-visual-edges-%E2%80%93-episode-34/





In processing, the central nervous system does route control. It controls the pathway of Nerve impulses going the CNS. It is the role of the synapses to regulate this. This process illustrated above is called lateral inhibition. The more stimulated area on the retina inhibits the response of the less stimulated.

The neuron class that starts this processing are horizontal cells. These cells run laterally. Horizontal cells that are involved in the synapses where light is intense send out inhibition to cells that are involved in the synapses where light is not as intense.

On center, off surround ganglion cells

The ganglion cell in this example (G) makes synaptic connections with 2 bipolar cells (B). These bipolar cells make synaptic connections with 4 rods (R). That defines the center of that ganglion cells receptive field. It is the connection that goes from receptor to bipolar cell to ganglion cell.

If a spot of light stimulated in the center, it strikes the receptors which hyperpolarizes and causes the “on” bipolar cell to be depolarized, which then releases NT to the Ganglion cells and we get a burst of Nerve impulses in the axons of the Ganglion cells.

If a spot of light stimulates Rods in the surround of the ganglion cell’s receptive field (not directly connected to that ganglion cell), it causes hyperpolarization of those rod cells. The surround receptive field's connections are not directly with the ganglion cells, but via horzontal cells (H).In the surround response, the light stimulus strikes a rod, and the rod sends NT to bipolar cells which hyperpolarizes and reduces it's NT release. This results in the horizontal cells inhibiting the ganglion cells and this is called lateral inhibition.

The ganglion cells have a response called a post inhibitory

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http://www.interactive-biology.com/1913/on-center-off-surround-ganglion-cells-%E2%80%93-episode-35/

http://www.interactive-biology.com/1913/on-center-off-surround-ganglion-cells-%E2%80%93-episode-35/





rebound, which means that after they are inhibited the actually depolarize many times above firing threshold and you get a burst of Nerve impulses. This ganglion cell is described as having an on center response, but having an off surround response (it produces a burst of nerve impulses when the light goes off from the surround).The surround receptive field includes all the receptors that are not connected directly to the bipolar cell but via horizontal cells.

“On” bipolar cells get stimulated when it gets NT from receptor cells. Off bipolar cells get inhibited when it gets NT.







PHONORECEPTION

Sound travels at about 800ft/sec. It dies out because it's a point source. The amount of energy goes down as the distance from the sound source increases, because the same amount of sound is spread over a greater area. Another reason for the decrease in energy is because some energy is lost as heat.

The wavelength determines the pitch of a sound. It is the distance between two points with the same density in a cycle. Shorter wavelengths give higher pitch sound and longer wavelength give a lower pitch sound. The unit for frequency is Hz (cycles/sec). Ideally, human hearing responds at a range between 20-20,000 Hz. Speech definition happens at high frequencies. Sounds travels through elastic (compressible) mediums, e.g. Air.

The structure of the mammalian earExternal ear (Pinna) - focusses sound down into the ear.Middle ear - Begins with the tympanic membrane and includes the ossicles (maleus, incus and stapes). There is an opening to the Eustachian tube which goes down to the mouth cavity (usually closed). Tympanic cavity.Inner ear (encased in bone) - Stapes connects to the inner ear via the oval window.

Cochlea (where the receptors are located, where hearing really starts)Round window. The inner ear is fluid filled.

TRANSFER OF SOUND WAVES TO THE INTERNAL EAR

When sound waves hit the tympanic membrane, it vibrates. This causes the bony ossicles to vibrate, which causes vibrations in the fluid of the internal ear. This bony cavity is filled with fluid. When the oval window moves in, it creates a pressure in the internal fluid and this pushes the round window out. The whole purpose of this whole apparatus (minus the semicircular canals for balance) is to get the vibrations into the fluid of the internal ear and it is these vibrations that lead to our perception of sound.

The middle ear is a closed cavity. When the pressure on the outside of the tympanic membrane is larger than the pressure in the middle ear, the tympanic membrane moves in. This makes it necessary for the Eustachian tube to open to equalize the pressure so that the tympanic membrane doesn't "pop". Fluid is much less compressible than ear. It takes more energy to create pressure waves in fluid. Because of this, it is necessary for impedance matching to happen in the internal ear.

Impedance matchingThere are two ways that impedance matching is accomplished in the ear:

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http://www.interactive-biology.com/1916/an-overview-of-the-mechanism-of-hearing-%E2%80%93-episode-36/

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http://www.interactive-biology.com/1919/how-sound-is-transferred-to-the-inner-ear-episode-37/

http://www.interactive-biology.com/1919/how-sound-is-transferred-to-the-inner-ear-episode-37/





The tympanic membrane is 18.6 times larger than the oval window. This takes all of the pressure creates over the whole tympanic membrane and focus it down on a smaller surface. This will create a much bigger force on the oval window.The ossicles are a system of levers. There is a ratio of the maleus to the stapes of 1.3 to 1. The maleus moves 1.3 times as much as the stapes. This also gives you an increase in force

These two processes together impedance match the air outside to the water inside

The function of Cochlea

The basilar membrane extends throughout the cochlea. It is narrow nearest to the oval window, and gets progressively wider and has natural frequencies along the basilar membrane. The narrow end bounces up and down in response to high frequencies, and the wider end response to lower frequencies.

When the oval window moves in as a result of a sound wave, the vibrations coming from the oval window go through the upper half of the cochlea. This causes a vibration in the basilar membrane. When the basilar membrane vibrates, the vibration goes through the membrane to the lower half, which is attached to the round window. When the oval window goes in, the round window goes out. The first stage of discriminating the pitch of sound is where we make the basilar membrane vibrate.

The basilar membrane is supported by bony ridges running down the cochlea. The basilar membrane is not wide enough to respond too the lowest pitch of sound that we hear at about 200 cycles per second. These low frequencies cause the entire basilar membrane to vibrate. This is interpreted as a low pitch sound in the brain.

Cochlea and Organ of CortiScala vesibuli/vestibular canal gets its vibrations from the oval window. The scala tympani is the lower half. At the end there is direct communication between the scala vestibuli and the scala tympani. This opening is called the halocotrema. The fluid in the scala tympani and the scala vestibui is the same. It is continuous.

The reissner's membrane separates the vestibular canal and the cochlea duct. It is transparent to sound. The scala vestibuli and the cochlear duct respond to the oval window in the same way. The fluid in the cochlear duct is different. It is endolymph, not perilymph. (This difference is crucial. This endolymph is higher in K.) So, sound waves makes the basilar membrane vibrate up and down, transferring the vibrations to the scala tympani.

ORGAN OF CORTI

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http://www.interactive-biology.com/1933/how-we-hear-different-pitches-episode-38/

http://www.interactive-biology.com/1933/how-we-hear-different-pitches-episode-38/

http://www.interactive-biology.com/1939/the-function-of-the-organ-of-corti-episode-39/

http://www.interactive-biology.com/1939/the-function-of-the-organ-of-corti-episode-39/





The organ of corti is located on the basilar membrane. This organ has some very important structures.Tectorial membrane is a very important structure. It is located on the organ of corti and extends all the way along the cochlea.Hair cells are the "most important" cells in the ear. They are cells which sit in the organ of corti. We have an inner row of hair cells, and 3 outer rows. They have steriocilia.

All other cells have a supportive function.

Branches of the acoustic nerve actually make synaptic connections with the hair cells. There are 4 rows of hair cells:

The inner row are the receptors for hearing. There are about 15,000 hair cells in the inner row.3 outer rows. There are about 32,000 hair cells in the outer row. These are involved in modulating the response of the organ of corti to sound. They are not the actual receptors even though they look like the inner row.

Mechanics of vibration (movement of the basilar membrane).

The basilar membrane vibrates up and down. This makes the organ of corti do the same kind of vibration, but as the organ of corti goes up, it makes the tectorial membrane vibrate "like a windshield wiper". It moves up and down but also laterally.

The steriocilia (hair) of the hair cells are in contact with the tectorial membrane, which means that the steriocilia of the hair cells are being tweaked back and forth by the tectorial membrane. It is the tweaking of the hair cells that leads to hearing. As the organ of corti moves, the steriocilia are deformed.

The scala vestibuli and the scala tympani contains perilymph. The cochlear duct has endolymph. Endolymph has a very high K+ concentration and the organ of corti and hair cells are in endolymph.

The steriocilia are connected together in pairs. There is a long cilium and a shorter cilium and a bridge between the two cilia. The short cilium has mechanically gated K channels. As these hair cells get

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http://www.interactive-biology.com/1956/the-role-of-hair-cells-in-hearing-episode-40/

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tweaked, that causes the channels to open. This will lead to an influx of K+ into the hair cell, which produces a receptor potential. The receptor potential is transferred electrically down to a place with synaptic vesicles and creates an EPSP in neurons that make up the Auditory nerve.

The receptor potential opens K+ gated Ca2+ channels. This does 2 things:Increases receptor potential.Increases neurotransmitter release directly.

Recruitment is a result of individual receptors having different thresholds. A very low intensity of sound only causes a response in some hair cells. As you increase the intensity of stimulation, this will result in a response in more receptors. In other words, more receptors are “recruited”.

There are 2 ways of sensing intensity of the stimulation:Individual receptors responding more vigorouslyMore receptors responding

There is a maplike relationship between the auditory cortex and the receptors. The organ of corti projects on to the auditory cortex in a maplike fashion. High frequencies that are caught in the region closes to the oval window excite the area in the auditory cortex more anteriorly.

The Muscular System

Vertebrate skeletal muscle Motor neurons leave spinal cord through ventral root and connect to muscle cells via synaptic connections. Motor neurons make connections to more than one muscle cell. When a motor neuron release ACh, all muscle cells that receive input from that motor neuron will respond. This is called the motor unit - a unit of muscle contraction.

When one neuron fires, only the cell(s) that are connected respond. If you want to have very fine contractions like in the eye, you want to minimize the amount of muscle cells that are connected to a motor neuron. In really fine contractions we have 1 motor neuron to 1 muscle cell.

On the cortical map, you can see which part of the cortex is connected to which part of the body. We find that the part that controls the hand has a large portion of the cortex, and the part for the feet is small. This is because there is a very fine degree of control when it comes to the hands because there is much more controlled motion with the hands and fingers.

The membrane around the muscle cell is called the sarcolemma. There are a number of nuclei in each muscle cell (polynucleated). Muscle cells are so long that you need more than 1 nuclei to furnish it with the DNA and other machinery that are necessary to keep muscle cells running.

The boutons of the motor neuron sits in a depression of the muscle. This depression is called a gutter. The muscle membrane here has folds, and wed find the Acetyl choline (ACh)receptors in the folds of the muscle membrane.

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http://www.interactive-biology.com/2012/an-introduction-to-skeletal-muscle-contraction/

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The units in the muscle cell are bundles of myofibril. Myofibrils are made up of actin (thin filaments) and myosin (thick filaments). These 2 proteins form the bulk of the myofibril.

There are 3 types of arrangements in the bundles:Only thin filamentsOnly thick filamentsboth filaments - One thick filament is surrounded by 6 thin filaments.

A myofibril is made up of sacromeres. Thick filaments overlap thin filaments. The distance between 2 Z lines is 1 sacromere.

There is a sarcoplasmic reticulum run around the muscle. At every place you have a Z line, the sarcoplasmic retiticuli go deep into the muscle. There are also T tubules running around the Z line. The terminal cisternae is a part of the sarcoplasmic reticulum that stores Calcium. It runs very close to the T tubules. This proximity is very important.

Within the sarcoplasmic reticulum there is a protein which binds calcium when it comes in. On the T tubule there is a protein (Dihydropyridine receptor) that binds to another protein called the Ryanodine receptor (on sarc membrane) that both act as calcium channels. This allows Calcium to go into the T tubule from the sarcoplasmic reticulum.

There are also pumps in the sarcoplasmic ret that pumps ca from the cytoplasm into the sarcoplasmic reticulum and is bound by a protein called calsequesterin.

Myofiber = muscle cell. Myofibril = units inside the muscle cell.

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http://www.interactive-biology.com/2032/how-the-release-of-calcium-ions-results-in-muscle-contraction-episode-42/

http://www.interactive-biology.com/2032/how-the-release-of-calcium-ions-results-in-muscle-contraction-episode-42/





The Sliding filament theory

Actin is made up of thin filaments and myosin is made up of thick filaments. Actin filaments is associated with 2 other proteins: Troponin and tropomyosin. Myosin have "heads" radiating in different directions as shown below.

Because myosin and actin are interdigitated, the heads have binding sites on the actin filaments. When the muscle is at rest that area is not available. The tropomyosin protein covers the area where the heads bind. When the muscle gets stimulated and the Ca2+ is released, Ca2+ is taken up by troponin. When troponin binds ca, tropomyosin changes its conformation and move out of the way, exposing the binding site. Myosin heads attach to actin. When ATP gets broken down, actin and myosin slides across each other and we get muscle contraction.

When an impulse comes through the motor neuron, the impulse causes Ca2+ to get into the presynaptic vesicle, neurotransmitters get released, and bind to receptors on postsynaptic membrane. The post synaptic potential spreads.

The muscle membrane(sarcolemma) contains V-gated channels. This causes an impulse in the muscle, which is then propagated along the sarcolemma, and goes via the T tubule system deep into the muscle cell. The dihydropyridine receptor gets stimulated, which then activates the ryanodine receptor.

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This channel opens, Ca2+ is released. Ca2+ binds to troponin, causing a conformational change in the tropomyosin. Actin binds to myosin, ATP is hydrolyzed and the muscle contracts.

Molecular structure and function of sarcomere

Thick myosin filament Made up of individual subunits that are the myosin units. The heavy meromyosin is made up of a head and a tailpiece.The light meromyosin has only a tailpiece.

There are 2 places where movement takes place in this unit. The head can flex along with the tail of the heavy meromyosin, which gives you the power for muscle contraction. However, the contraction depends on connection. It is pulling the actin. To do that the myosin head has to connect to the actin.

Thin actin filamentMade up of g actin monomers. A cross bridge from the myosin will connect to a special site on the actin monomer. The whole actin filament is called f actin.

It is the availability of the binding sites that starts the contraction. There is a protein called tropomyosin that lays right over the binding site, making the binding site unavailable. There is a third protein complex called troponin (has 3 subunits), which is a calcium receptor. Troponin binds 4 calcium ions in order to do its thing.

The terminal cisternae releases Ca2+ when we have a action potential. The Ca2+ binds troponin, causing a change in conformation of the tropomyosin, which causes it to move. Then binding sites on actin are available, and as soon as this happens, contraction begins. The myosin can't cross bridge with the actin until the binding site is available. The head of the myosin filament is phosphorylated, putting it in the high-energy state (resting).

As soon as the binding sites become available, the myosin forms a cross bridge with the actin. The next step is the power stroke (flexing of the head). The phosphate is removed and the myosin goes to its lower energy state and we get the power stroke.

These cross bridges stay until we have energy. When we add ATP, the cross bridge breaks. Binding a new ATP breaks the cross bridge. In order to put it back to it's resting state (energized), the head has to be phosphorylated by the ATP.

When Ca2+ gets pumped back into the terminal cisternae, it stops the effect of Ca2+ on the muscle and muscle contraction ceases.

Energy Source for Muscle Contraction

The energy source for contraction is ATP. Muscle is very richly supplied with mitochondria. Glycogen is a storage source of energy. It is a polymer of glucose units. The largest energy storage in the muscle is in glycogen. Another place of glycogen storage is in the liver. Glycogen has to be broken down into glucose in the liver taken to the muscle via the bloodstream.

In anaerobic glycolysis, you are re-oxidizing NADH by reducing pruvate into lactic acid.







Then the lactic acid is being reoxidized to pyruvate, which then goes through the Krebs cycle to yield ATP. The excess goes through neogenesis to regain glucose.

You cannot do anaerobic glycolysis with fatty acids. Our major ATP source is electron transport and is oxygen dependent. We don't store ATP. We store molecules that can make ATP. However, in the muscle this is different. Creatine can take up a phosphate and get a higher energy bond than ATP. At rest ATP can phosphorylate creatine to creatine phosphate. When contraction is happening, Creatine phosphate can phosphorylate ADP to get ATP. If things get really tough, 2 ADP can be converted into ATP and AMP. The most important thing for contraction here is being able to make ATP available.

Types of muscles cellsMonoterminal - Each muscle cell has a single motor end plate. All monoterminal muscle cells have a membrane that generates an all or nothing Muscle impulse.Slow phasic: A phasic muscle cell is one that is designed to contract with strength but not for a long time. Has a relatively slow onset of contraction. It also has many mitochondria and is thus a heavily aerobic muscle. So in this muscle we have lots of fat. Tetanus occurs at a very low frequencies of stimulation.Fast phasic: This varies between having few mitochondria and no mitochondria. It is primarily anaerobic, so it's energy comes from carbohydrates through anaerobic metabolism. It is the “white meat” and fatigues easily.Fast phasic oxidative: Have many mitochondria and they don't fatigue as easily. They contract very rapidly (fast twitch). Takes a very high frequency of stimulation to achieve tetanus.







The Circulatory SystemHuman Physiology - By Leslie Samuel






The Heart and Major Vessels

The blood goes through the heart twice and the valves are crucial. The heart is the pump and it has two halves. 1 half (right) sends the blood to the lungs and the other (left) to the rest of the body. There is an alternating rhythm of contraction with the atrial and the ventricular contractions.

Blood comes in from the body via the vena cava and empties into the right atrium (see figure above). Blood moves from the right atrium through the tricuspid valve (One of a pair that we call the atrioventricular valves [A.V. Valves]).

The blood moves through the tricuspid valve to the right ventricle. Then it moves through the pulmonary valve (semilunar valve) to the pulmonary artery (without much oxygen). Then the blood goes through the lungs to the pulmonary veins and then to the left atrium, through the mitral valve (a.v. valve) to the left ventricle (most important - creates pressure for circulation). Then it goes through the aortic valve to the major artery, which is the aorta, and then to the rest of the body.

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Control of the Heart Beat

The Pacemaker The pacemaker is a group of specialized muscle cells that do not contract. It is found in the right atrium right where it joins with the superior vena cava and is called the sino atrial (S.A.) node. The sino atrial node cells set the rythm for the beating of the heart.

There is no resting potential in the pacemaker cells because the Membrane Potential never remains stable. There is first a higher Na+ conductance than K+ conductance, and Na+ moves through special channels into the pacemaker. So the potential continuously moves towards firing threshold. Late in the cycle Ca2+ channels open and potential continues to move towards threshold, and we get an action potential much longer than we've seen in the past. Then K+ conductance decreases. It is an all or nothing impulse, but it just lasts longer, and we have no resting potential.

How is the heart rate regulated in terms of speed?

Regulation happens through 2 substances that are produced by the autonomic nervous system. ACh (parasympathetic) - decreases heart rate. When ACh increases, that causes an increase in K+ conductance. K+ hyperpolarizes the cell, making it harder for depolarization to happen. The effect of this is a decrease in heart rate.Epinephrine (sympathetic) - increases heart rate. With normal epinephrine levels, we have a relatively high Na+ and Ca2+ conductance and a low K+ conductance. If epinephrine levels increase we get a higher Na+ and Ca2+ conductance, thus depolarization happens faster, which results in a higher heart rate.

The Sa node is a group of specialized muscle cells that don’t contract. All they do is generate the electrical rythm for the rest of the heart - the pacemaker potential. The SA node cells do not have a stable resting Em. It is always fluctuating.

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Pacemaker Cell Pacemaker Cell Pacemaker Cell

Na+ K+ Na+ Ca2+ K+ K+Na+

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http://www.interactive-biology.com/2210/045-the-pacemaker-potential-of-the-sa-node-and-the-av-node/

http://www.interactive-biology.com/2210/045-the-pacemaker-potential-of-the-sa-node-and-the-av-node/

http://www.interactive-biology.com/2222/046-how-adrenaline-and-acetylcholine-affect-heart-rate/

http://www.interactive-biology.com/2222/046-how-adrenaline-and-acetylcholine-affect-heart-rate/





At the lowest potential, the SA node cells are leaky and allows Na to leak in. This depolarizes the membrane. When it gets to firing channels, V-gated Ca channels open and you get a very fast depolarization to the peak of the action potential. At the peak, K+ channels open. When K channels open, K+ leaks out and you get hyperpolarization. Then the process happens again.

The SA node does not depend on the nervous system for the rythm, but they do receive innovation from the nervous system (autonomic). The parasympathetic fibers released ACh and the sympathetic fibers release Epinephrine.

Epinephrine makes Na+ and Ca2+ channels very leaky. This results in faster depolarization. Thus, if we increase Epinephrine levels, we get an increase in heart rate. This is called positive chronotropy because the speed is increased. Positive inotropy means that each heartbeat is stronger.ACh makes K+ channels sensitive, and slows down heart rate. This effect is negative chronotropy and negative inotropy.

The signal travels from the SA node at a speed of 1m/s to the AV node at a speed of 0.05m/s (slows down).Then it travels down the AV bundle at a speed of 4m/s to the purkinje fibers at and is then carried to the rest of the heart muscle. This delay in speed between the SA node and AV node allows for the ventricle to get full with blood before it contracts.

The cells from the AV node can become a pacemaker if the Signal does not get from the SA node to the AV node. The SA node dictates because it has the fastest spontaneous activity, so it serves as the pacemaker. But if it doesn’t work, the AV node, which has the next fastest spontaneous activity, will act as the pacemaker.

Some organisms have a neurogenic heart. We have a myogenic heart.

1. Sinoatrial node2. Atrioventricular node3. Bundle of His4. Left bundle branch5. left posterior fascicle6. Left-anterior fascicle7. Left ventricle8. Ventricular septum9. Right ventricle10. Right bundle branch

Electrical conduction system by J. HeuserHeart by Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional Media







Isovolumetric contraction of the ventricle

After the atria contract, the QRS wave appears. QRS is the stage of ventricular depolarization. At this stage, the ventricle don't immediately change in size. Since the Valves are all closed, this builds up pressure in the ventricles. This is when the force that goes to pump blood is generated.

The systolic pressure comes from 0 to about 110 mm HG. This is a lot of tension/pressure. It becomes so much that it gets higher than the aortic pressure. When the pressure gets above the aortic pressure, it opens the pulmonary valve and the aortic valve. This marks the end of the isovolumetric contraction of the ventricle.

Ventricular contractionThe stroke volume is the amount of blood that is ejected from the heart. The stroke volume is about 70 ml. End diastolic volume (EDV) is approximately 130 mL. The residual amount of blood that remains is approximately 60ml (End systolic volume: ESV). Ejection fraction = SV/EDV and is approximately 53% at rest and 90% during exercise.

When Ventricles expand, the pressure becomes less, then AV valves open.

RegRegulating Stroke Volume

If the heart is to regulate how much blood it's going to pump, it has to be able to regulate EDV and ESV. There are 3 ways to increase the EDV:

Increase ventricular contraction (epinephrine from sympathetic neurons- positive inotropy). This in essence decreases ESVIncrease the amount of time for fillingIncrease the amount of blood returning from the rest of body (venous return).

Increasing Venous Return with The skeletal muscle pumpThere are skeletal muscle pumps that surround our veins. If you are exercising your muscle they contract in a way that forces more blood through the veins faster. So the activity of the skeletal muscle increases venous return

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http://www.interactive-biology.com/2368/051-isovolumetric-contraction/

http://www.interactive-biology.com/2368/051-isovolumetric-contraction/

http://www.interactive-biology.com/2226/047-action-potentials-and-contraction-in-cardiac-muscle-cells/

http://www.interactive-biology.com/2226/047-action-potentials-and-contraction-in-cardiac-muscle-cells/

http://www.interactive-biology.com/2265/048-how-to-read-an-electrocardiogram-ecgekg/

http://www.interactive-biology.com/2265/048-how-to-read-an-electrocardiogram-ecgekg/

http://www.interactive-biology.com/2283/049-what-stroke-volume-is-and-how-to-calculate-it/

http://www.interactive-biology.com/2283/049-what-stroke-volume-is-and-how-to-calculate-it/





Improving stroke volume by decreasing ESVIncreasing the pressure generated during systole. (Influenced by Catecholamines)Improving pulmonary and aortic pressure by lowering the pressure. This is accomplished by exercise also.

The Frank-Starling mechanismWhen the heart is stretched due to being more filled with blood, that enhances the actin myosin overlap in a way that causes the heart to contract stronger. If there is less blood in the heart, the tension will be less and the contraction will be less. The Frank-Starling mechanism states that the heart will adjust itself for whatever volum you give it.

Regulation of Cardiac Output

C.O. = Cardiac OutputH.R. = Heart RateS.V. = Stroke Volume

Stroke volume is the amount of blood ejected per stroke. End diastolic volume is the amount of blood in the left ventricle before it contracts (isovolumetric stage). It is the maximum amount of blood. End Systolic Volume is the amount of blood remaining in the heart after contraction.

Stroke volume = E.D.V. - E.S.V. - These 2 values are regulated independently Regulation of E.D.V.

Skeletal muscle pump - This increases venous return, which in essence is increasing E.D.V.Increased sympathetic activity, which means that there is an increase in the availability of epinephrine and norepinephrine. Epinephrine is delivered to body tissue. It comes from the adrenal

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C.O = H.R. * S.V.

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What happens to the way Cardiac output takes place as you do exercise?

If you start off in a state of poor fitness, but then you start doing a good Cardiovascular exercise regularly, you find that reaching a certain level gets easier an easier. This does not mean that your muscles needs less blood and oxygen. It means that one of the major things that happens during training is that the heart ejects more blood with each contraction. This refers to the stroke volume. Resting heart rate also drop. Fit athletes may have very low resting heart rates.



http://www.interactive-biology.com/2290/episode-50-regulating-stroke-volume-skeletal-muscle-pump-and-frank-starling-mechanism/

http://www.interactive-biology.com/2290/episode-50-regulating-stroke-volume-skeletal-muscle-pump-and-frank-starling-mechanism/

http://www.interactive-biology.com/2507/053-cardiac-output/

http://www.interactive-biology.com/2507/053-cardiac-output/





medulla, which is sort of a reservoir and is full of capillaries. The source of norepinephrine is the same as epinephrine. It is delivered directly to the tissue it affects. So epinephrine and norepinephrine can be delivered to the same tissue, but by different means. Most of the time they have the same effects.

Increased Epinephrine and norepinephrine release also increases venous tone. There is a smooth muscle layer that contracts and is influenced by epinephrin and norepinephrine. With increased venous tone the walls of the veins shape up a little and make it easier for blood to flow.

These 2 things influence the amount of blood returning to the heart. You get increased venous return, which in essence increases end diastolic volume.

Regulation of E.S.V.There is only one general way to change E.S.V and that is to change how much the ventricle contracts. The more it contracts, the smaller the E.S.V. is. There are two major sources for changes in E.S.V.

Autonomic nervous system affect - This means that there will be an increase in the availability of epinephrine and norepinephrine. These are delivered in the same way as in regulating E.D.V. In this case they also have the effect of increasing contractility. This is a function of the increased availability of Ca2+.The stretched ventricular muscle will enhance contractility, which means more cross bridges. -> Stronger contraction. This is called the Frank-Starling mechanism. So this is a direct result of E.D.V. because this stretches the ventricle. So we have looked at the regulation of stroke volume.

Blood pressure regulation

The pressure in the aorta fluctuates. The pressure in the aorta is the lowest the instant before the aortic valve opens. This is the diastolic pressure. As the ventricle contract, the pressure in the aorta is increased to a peak and this is called systolic pressure.

When we talk about regulation of pressure we have to remember that the pressure in the large artery (aorta) is increasing.

Pulse pressure = systolic pressure - diastolic pressure

So the numbers that we typically hear are 80mm Hg and 120mm Hg, so the typical pulse pressure is approximately 40mm Hg.

Mean arterial pressure (MAP) What MAP does is to find the area under the curve, define a rectangle with the same total area and define the value of the top of the rectangle as MAP. This turn out to be easier to calculate than trying to define the area under the curve. We can do so with the following formula:

MAP = DP + 1/3P.P

ACh is involved in regulating heart rate, but not Stroke Volume

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http://www.interactive-biology.com/2515/054-blood-pressure-and-mean-arterial-pressure/

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This, once again is the average pressure in the large artery

A second formula for calculating MAP

MAP = CO * PR

Peripheral Resistance (PR) is the total resistance to blood flow in the body. The major arteries and smaller arteries have very thick walls, and are made to be flexible. However, these arteries tend not to constrict or dilate actively. They don’t get bigger or smaller on average. If there was something that changed the diameter, resistance to flow would change. This means that the arteries aren't the place to change the cross sectional diameters.

Capillaries are histologically made up of single epithelial cells. They are only one cell layer thick. So there isn't any muscle or connective tissue. Capillaries aren't the place either.

So this only leaves one place - Arterioles. Arterioles contain an inner circular layer of smooth muscle. This layer can contract or relax leading to constriction or dilation. This affects peripheral resistance, which increases with constriction and decreases with dilation.

Surprisingly, we have twice as much circulatory volume in our body than blood. Most of that circulatory volume is in the capillary beds. So this means that some capillary beds have to be shut out completely. There are two types of medical situations in which our blood "gets lost".

Fainting - not enough blood going to the brain. When this happens, you lay them down on the grown and elevate the legs so the blood can go to your heart and especially to the brain. Fainting is a result of a system-wide vasodilation. So the blood pools in your lower extremities. In a really serious vasodilation, the result is shock. Blood pressure drops dramatically for a long period of time. The heart will quit contracting if it doesn’t have enough blood to pump. This can sometimes be irreversible.

Regulating Peripheral Resistance

Alpha receptors (found on the arterioles) have a 7 transmembrane sequence (2nd messenger). It is mainly responsive to norepinephrine. This comes from sympathetic neurons released at the site. these contact the receptor. There is a G protein that activates phosphatidyl inositol, which releases IP3, which causes release of Ca2+ from the cisternae and the sarcoplasmic reticulum. This causes vasoconstriction.

The smooth muscle cells are also supplied with beta2 receptors. They are some distance from sympathetic nerve endings. Thus it will be much more responsive to epinephrine. So here is the sequence of events. The epinephrine contacts the beta2 receptor (7 transm). This activates a g protein, which activates adenylate cyclase, which produces cAMP, which activates Ca2+ pumps (into cisternae). This causes a decrease in Ca2+ levels, leading to vasodilation.

There is another kind of receptor called a beta1 receptor. They are located in the cardiac muscle. In this case, the causative agent is mainly norepinephrine, because these are near nerve endings. It is also receptive to epinephrine, but not as much. This causes an increase in cAMP, which then causes the

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increased availability of Ca. This gives stronger contraction of cardiac muscle cells. ESV decreased because heart muscle cells contract stronger.

High levels of norepinephrine will activate alpha receptors leading to vasoconstriction. So vasodilation happens best at moderate levels. This does not mean that when the level of norepinephrine is high that the beta2 receptors are not activated. It just means that both are activated, but the alpha effect predominates. When you are exercising a lot, you want blood flow to muscles to increase. So what you want to do is to activate the beta2 effect in your muscles. During heavy exercise, moderate levels of epinephrine are pumped out. High levels are saved for emergencies. This keeps blood pressure high enough, so that high levels of blood will go through your heart and supply the brain with the necessary nutrients.

There is another influence that we need to emphasize because of its importance and that is the control by local metabolites. These things will typically result in vasodilation. Lets say you’re out jogging. The greatest energy use is in the legs. This uses ATP by using oxygen and producing CO2. This increases H+ levels. This muscle can continue being active because as a result, local metabolites causes vasodilation in local areas.

Blood viscosity

If the blood gets thicker, it gets harder to pump, but we are not going into that.

Angiotensin and MAPThere is a protein circulating in the blood normally called angiotensinogen. This protein is inactive in this form. If there is a decrease in MAP, the kidney senses this and will (via the juxtaglomerular apparatus) release another protein called renin. This is an enzyme that acts on angiotensinogen. It breaks off part of the inactivating polypeptides.

When this happens, It then becomes angiotensin I, which is slightly active. This then goes out to the body. At various places in the circulatory system especially in the lungs there is this converting enzyme called angiotensin converting enzyme (ACE). This converting enzyme changes angiotensin I to angiotensin II, which is the most potent vasoconstrictor in the body by causing the smooth muscle in the arteriole to contract. This was first thought to be an emergency regulator, but now it is seen to be normal.

There is a group of drugs called ACE inhibitors that block ACE. Having high blood pressure is a major health problem. About 85% is not yet understood, but we do know that the most common problem is that there is too much vasoconstriction.

Pressure reflexes

Watch Video

Watch Video





http://www.interactive-biology.com/2553/057-pressure-reflexes-and-mean-arterial-pressure/

http://www.interactive-biology.com/2553/057-pressure-reflexes-and-mean-arterial-pressure/





For you to regulated body processes, your body has to be able to know how the body is currently functioning. This can result in short term/immediate regulation via the nervous system.

How does the nervous system know what the blood pressure is?

Baroreceptors These receptors are located in the arteriole system and they sense blood pressure. They are found primarily in 2 locations: The aortic body and the carotid body.

The aortic body is a thickening in the aorta. Its firing rate increases in direct proportion with the amount of pressure in the aorta. These pressure receptors send nerve impulses to the medulla, which is the primary blood pressure regulating center. There are also connections up to the thalamus, hypothalamus an the cortex, but we are not going to go there.

With an increase MAP, we get increase in the rate of firing of the baroreceptors, which goes into the medulla. This is where we talk about pressure reflexes. This has 2 effects:

It increases parasympathetic activityIt decreases sympathetic activity.

This combination will cause a reduction in cardiac output. The decrease in sympathetic activity will cause a decrease in Peripheral resistance. With these 2 reduced, we get a decrease in MAP.

We started with an increase in MAP, and this response causes a reduction in MAP. This is why we call it a pressure reflex.

If we started with a decrease in MAP, this would lead to a decrease in parasympathetic activity, and an increase sympathetic activity. As a result, MAP would increase.

When we have high or low blood pressure the brain tries to adjust via the activity of the Medulla. Sometimes, we take drugs. Some drugs that are used affect CO, but this also affects how active you can be. Others influence PR by blocking Ca2+ channels. This causes vasodilation. Others blocks ACE. Then we don't get angiotensin II, and then we get an increase in vasodilation.

Long term regulation of MAP Long term regulation of MAP is accomplished by regulating blood or fluid volume. An increase in the fluid volume raises the resistance to flow. The most important long term regulation is accomplished by the kidneys. Another general approach is using a diuretic, which interferes with the absorption of water, and you decrease fluid volume.

The baroreceptors are not the only route into the medullary regulation. There are series of other mechanisms that we are going to mention very briefly:

Chemoreceptors - the are located in the same places as baroreceptors - both the carotid and aortic bodies and elsewhere. These chemoreceptors will detect an increase in CO2 levels, increased H+ concentration (as a result of increased CO2 because of Carbonic acid) or a decrease in O2. If one of these things happen, the result is an increased sympathetic activity. Clearly, each of these would indicate there is not enough blood in the area where the chemoreceptors are located.A receptors - There is an A receptor which responds to changes in heart rate. They then send signals to the medullary center, which will either cause an increase in parasympathetic or sympathetic activity depending on which is appropriate - whether it is necessary to increase or decrease heart rate.







B receptors - These receptors are excited by filling. These too send signals to the medullary center, which will then increase sympathetic activity. If you are running, blood is getting back to your heart faster because of the skeletal muscle pump. The B receptors send signals to the medulla, which will caus an increase in sympathetic activity, which increases heart rate. This also reduces ADH production and this will cause an increased urine output.C receptors - these innervate the junction between the right atrium and the vena cava. This can cause a medullary reflex, which can be either sympathetic or parasympathetic depending on what's appropriate. When secretory cells stretch, they released naturetic peptide, which results in a decrease in ADH, Renin, and aldosterone release, which increases urine production. The overall result is a decrease in MAP

Distribution of blood in the body When you are sitting, you are not flooding your muscles with blood. C.O. is not very high. While we are using our brain, it does require some blood, but not as much as during physical activity. As you become more active, blood goes to different places.

Resting C.O. is approximately 5L/min. This keeps you warm. When you start exercising, your cardiac output increases about 5 times and the distribution changes. This is caused by vasodilation in the muscles via beta II receptors/epinephrine, and also the local metabolites. So if you are jogging, your quadriceps and gastrocnemius muscles will get the most of the blood.

It is not smart to go swimming after you eat. If you swim, you are going to flood blood to your muscles. If you are digesting, there is a lot of blood trying to go there. The muscles that are being pushed hard don’t get enough blood and will cramp. Cramping is simply a runaway contraction, which probably means that there is too much Ca2+. If there is not enough ATP to run the Ca2+ pumps to pump the Ca2+ back out, we will get too much calcium. This results in cramping.

Pressure changes throughout the circulatory system







This graph shows a lot. Lets start with the left ventricle (top blue line). The pressure changes from almost 0 to over 120mm Hg. The very low pressure is necessary to allow blood to flow into the ventricles and the high pressure creates the pressure for circulation. When the blood gets into the aorta and large arteries, the pressure only drops so far.

You're arteries have 2 important components. a lot of elastic connective tissue and smooth muscle, which can both be stretched. When the ventricles contract, arteries stretch because it is full of blood. This stretched artery is storing the pressure from the ventricles. When the arteries relax, the aortic valve closes to prevent backflow into the ventricle. So the pressure in the arteries remain high because they are full of blood. The Arteries then constrict to drive blood to the vasculature of the body. As the blood moves out into the small vessels, the pressure drops. The blood is being forces out into smaller vessels.

The pressure in your large arteries hardly show any difference from place to place. So we can check blood pressure many places. As the blood moves into the smaller arteries, the blood cells bump against the edges and we get friction. We then see a rapid drop off in pressure to the arterioles. When the blood gets into the capillaries, there is no longer a fluctuation.

The smallest capillaries are where the greatest exchange takes place and blood cells move through them in a line. The blood is in these exchange areas for less than a second. Then the blood continues into the venules and into the large veins but the pressure is continuously dropping. The total cross sectional area is huge in the capillaries. The rate of flow decreases.

Watch Video

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The whole purpose of circulation is the movement of materials from one place to another. How does this movement of substances into and out of the capillaries happen?



http://www.interactive-biology.com/2500/052-the-cardiac-cycle/

http://www.interactive-biology.com/2500/052-the-cardiac-cycle/

http://www.interactive-biology.com/2568/058-net-hydrostatic-pressure-and-filtration-pressure/

http://www.interactive-biology.com/2568/058-net-hydrostatic-pressure-and-filtration-pressure/





Movement of material into and out of blood

Blood pressure = hydrostatic pressure. If there is a high pressure inside the capillaries and the walls have fairly large pours, fluids and small molecules will flow out of the capillary walls. This process is called filtration. These substances go into the tissue fluid. The concentration of small molecules going to the tissue fluid is the same as he concentration in the blood. This will lower the water concentration in the plasma, which means that we will have a setup for osmosis to occur. Water will them move into the capillaries.

Net hydrostatic pressure = Blood pressure - tissue pressure. (This is the pressure moving fluids in). The filtration pressure = net hydrostatic pressure - net osmotic pressure.

We have blood in an arteriole going into a capillary. As the blood goes into the capillary the H.P. goes down due to the large amount of friction. In other words the pressure that moves stuff out is decreasing. On the other hand, as water moves from the blood into the tissue fluid, the net osmotic pressure goes up. The part of the capillary bed nearest to the arteriole is where the net filtration pressure is the highest, and the part closest to the venule is where the net osmotic pressure will be the highest. The point in the middle where the 2 pressures are equal is called the dynamic center.

In high blood pressure situations, the H.P. is high and it drops across the capillary bed but you end up with more of the cap bed involved in giving off fluid to the tissue and a small region taking fluids in. This will result in a net dropoff of water into the tissue. This leads to an abnormal amount of fluid accumulation in tissue, which is called edema.

HUMAN CIRCULATORY DIFFICULTIES

Hypertension/high blood pressure The most common form is called essential (primary) hypertension. Causes:

Increased fluid volume in the body, which means increased blood volume. The cause of urine production is blood pressure. If you lower blood pressure significantly, urine production can drop to nothing. If you increase blood pressure, this will raise urine production very much. We tend to keep fluid volume normal at a normal MAP. A person with higher MAP regulates urine output around that MAP (graph). Another major cause is increased peripheral resistance. That would largely be because there is too much average vasoconstriction. Neurogenic - One of the major causes is that there is an overproduction of an anterior pituitary hormone called ACTH, which results in an overproduction of the hormone cortisol, which can lead to hypertension.

Common ways of treating hypertension is by either increasing vasodilation (Ca channel blockers an ACE inhibitors), or to reduce cardiac output (beta blockers - reduce heart rate). The third approach is to reduce fluid volume (diuretics).

Atherosclerosis Plaque can be deposited in large arteries. This is called atherosclerotic plaque. High cholesterol levels in the blood, especially in low density lipoprotein or LDL cholesterol. There is another form called HDL, which is good for you.







When this stuff accumulates in the large arteries, one of its favorite locations is the coronary arteries, which are the arteries that feed your heart. There are 5 or 6 of these. This is usually the case with bypass surgery. They also tend to deposit in the carotid arteries (feed the brain). Both of these situations lead to a high probability of thromboses. An embolus is a floating blood clot or some other particles. When that comes to lodge in a particular place, it becomes a thrombus.

The most common place is in the coronary artery, which can lead to a heart attack because the heart is deprived of blood. It is more likely to lodge in a coronary artery that's stuffed with a plack deposit. If the thrombus lodges in one of the major arteries going to the brain this can result in a stroke.

Atheriosclerosis can lead to an even more serious stage, especially with high bp. This stage is called arteriosclerosis. Sclerosis is hardening. This results from calcification of the plack. It becomes hard and rigid. When coroners squeeze the arteries of older corpses it can sound like twigs breaking.







The Respiratory System

Transport Of Gases

Cellular Respiration Equation: C6H12O6 + 6O2 -> 6CO2 + H2O

One of the main functions of blood is taking Oxygen to and removing CO2 from the tissues.

Oxygen transport. The solubility of oxygen in water is .3 mL to 100mL plasma. On the other hand, whole blood carries 20mL per 100mL. This difference is due to the presence of hemoglobin.

Watch Video



http://www.interactive-biology.com/2587/059-an-introduction-to-the-respiratory-system/

http://www.interactive-biology.com/2587/059-an-introduction-to-the-respiratory-system/





Oxygen transport occurs primarily via red blood cells, which have hemoglobin. Hemoglobin is made up of 2 different types of protein chains. 2 alpha and 2 beta chains, which are very similar. These 4 chains together make up a hemoglobin molecule. Within hemoglobin there is a crucial subunit called a heme group. This heme group with a central ion associates with an Oxygen molecule. It is not a covalent bond. There is a physical attraction (charge). The ion can take on and give off an oxygen molecule very easily.

One oxygen can associates with each heme group. So a hemoglobin molecule can associate with up to 4 Oxygen molecules. In associating with oxygen, the individual units change in position with respect to each other. As O2 comes in, the actual hemoglobin molecule changes shape, increasing affinity for oxygen.

Deoxyhemoglobin has a relatively low affinity for O2. As it begins to load up with Oxygen, the affinity for oxygen increases. Hemoglobin, in its oxygenated state has a higher affinity for O2. When the hemoglobin leaves the lungs and goes to the body, we see the reverse effect. The hemoglobin gives up its oxygen. The shape changes in a lower oxygen environment reducing affinity for oxygen and causing oxygen to be delivered (blue line).

Watch Video



http://www.interactive-biology.com/2631/060-hemoglobin-and-the-oxygen-dissociation-curve/

http://www.interactive-biology.com/2631/060-hemoglobin-and-the-oxygen-dissociation-curve/





The relationship between the transfer of O2 and the amount of O2 in the environment is shown in the oxygen disassociation/association curve (above .

The partial pressure of O2 (PO2): this is a measure of how much O2 is available in that particular environment. The air that you breath is 20% O2. If the pressure of the air is at 760 mm Hg, then the PO2 will be around 152 mm Hg. Since the air in the lungs is saturated with water and water takes up some of that, the actual value is around 110 mm Hg. The curve expresses the level of saturation of hemoglobin based on the amount of O2 in the environment. It is S shaped. When hemoglobin is in the lungs, it will saturate, but when it goes to a tissue, it drops, and will deliver O2.

The Oxygen Dissociation Curve

The crucial factor is AFFINITY. The greater the affinity the less oxygen it takes to load hemoglobin up. As the tissues and the blood plasma pH becomes more acid, hemoglobin affinity is reduced. Since that acidity is going to happen in the tissues, this means that the tissue that's more acidic will get more oxygen.

Blood goes from the heart, to the lungs, back to the heart, and then out to the tissues. When it goes through tissues, it only goes through one set of capillaries. It comes to the tissues loaded with oxygen. The more acidic the tissue environment, the more the hemoglobin unloads oxygen.

The tissue becomes acid due to the production of CO2, which leads to Carbonic acid formation. Hemoglobin loads up at a PO2 of about 100. In the muscles there is a molecule called myoglobin, which is very similar to hemoglobin. However, it only has one heme group instead of 4. When we look at the oxygen dissociation curve of myoglobin we see that it loads up at a lower PO2 than Hemoglobin. So when hemoglobin unloads O2, myoglobin readily takes it up.

Hemocyanin (found in Horshoe crabs) has an oxygen dissociation curve like myoglobin. It has a High affinity for oxygen. So this pigment has an easy time picking up oxygen, but a hard time delivering it. The tissue PO2 has to be very low.







Mice have high metabolic rates. They burn oxygen much more rapidly than we do. Animals that live at high altitudes have an oxygen dissociation curve shifted to the left. This means it loads up with oxygen more easily, but can't be as active because they have to create low PO2 in there tissues.

A mouse living at high altitudes will have an Oxygen dissociation curve shifted to the left. It needs to load up easily, but it can't be as active. If you find an organism of the same species living at sea level, the curve will be shifted to the right. This means that there is an important adaptation that occurs that depends on Oxygen availability.

Lets now look at how CO2 is transported.

CO2 + H2O <--> H2CO3 <--> H+ + HCO3-

We have CO2 going into the blood and Oxygen going into the tissue. The first reaction that happens is that 7% of the CO2 that we produced goes to the reaction above leading to the production of Carbonic acid. The blood buffers are good enough to handle that much carbonic acid. This stays in the plasma.Now, 70% of the CO2 goes through the following reaction inside the red blood cell forming H+ and HCO3- by the enzyme Carbonic anhydrase. This is where hemoglobin takes on another function. When oxyhemoglobin (HbO8) releases O2, it also picks up protons. In this case, hemoglobin is the buffer. This causes a problem.

The bicarbonate will go through the RBC membrane out to the plasma. This will increase the charge across the membrane and will stop bicarbonate from leaving if there isn't another mechanism for getting rid of it.

When bicarbonate leaves, Cl- comes in and takes care of the charge. This is called the chloride shift and depends on specific permeases for Cl- and bicarbonate ion. The process of transport can then continue.

The other 23% produces Carbamino Hemoglobin (HbCO2): CO2 + Hb (deoxyhemoglobin) <--> HbCO2. It never forms carbonic acid.

WHEN YOU GET TO THE LUNGS WE GET THE REVERSE OF ALL OF THIS: Oxygen is picked up and CO2 is delivered.

Respiratory Exchange: The exchange of gases between organism and environment.A planaria is a flatworm. It does not have a respiratory system. Because it's flat and thin, all or the cells are close enough to the environment.

Here are the requirements for a Respiratory Surface:Large surface area.It has to be moist - Gas exchange happens in solutionHas to happen near active cells or have easy acces to them - cells that are using oxygen and producing CO2

Watch Video



http://www.interactive-biology.com/2643/061-the-bohr-effect/

http://www.interactive-biology.com/2643/061-the-bohr-effect/





How do we fullfil those requirements? The respiratory surface of both lungs is about the size of a tennis court, which is pretty huge. Why not just put it on our back? Because moisture loss would be too big. The air that we breathe out is typically saturated with water. Our lungs are inside our bodies. Since they aren’t close to all of our active cells, we have to add a circulatory system. This respiratory area has to be highly vascular so that the blood is not very far away from the air.

The Human respiratory system

LungsOur lungs are elastic/stretchy. This is because of elastic connective tissue and a little bit of smooth muscle, but they can't be a muscular organ like the heart that themselves contract and expand. We have to have an elastic lung that is very thin and facilitates gas exchange.

The 3 Cavities:Intrapulmonary: inside the lungs. It is open to the atmosphere all the time. Thoracic cavity: The whole cavity that contains the lungs and heart. It is sealed.Pleural cavity: Bounded by the pleural sac. This sac has 2 layers: A parietal layer that lines the thoracic cavity and a visceral layer that covers the lungs. It is fluid filled, which acts as a lubricant.

Breathing involved an active change in the volume of the thoracic cavity, reducing and increasing its pressure. We are going to see how that happens. But before that, lets look at the actual structure in the lungs that supports gas exchange.

Trachea - main airway between the mouth and the lungs.2 major bronchi - large tubes, one going to each lungs.Bronchioles - small tubesAlveolar ductAlveolar sac - terminating the ductAlveoli - where the major gas exchange happens







The alveolar duct and sac are covered with a capillary network. The blood gets oxygenated and goes back via the pulmonary vein to the heart.

Pressure Changes During Respiration

If there is going to be pressure changes in the thoracic cavity there has to be volume changes.Thoracic cavity pressure changes

Diaphragm: The boundary between the thoracic cavity and the abdominal cavity. The diaphragm is kind of oval shaped. It is a band of muscle, and there is central connective tissue, which is strong but non-contractile. Its shape at rest is domelike.

Thoracic cavity wall: The external intercostal muscles - These are involved in inspiration. The internal intercostal muscles - These are involved in expiration.

Eupnea - normal/quiet breathing.Inspiration has to result in a reduced thoracic cavity pressure. So making the cavity larger does this. The cavity is made larger by 2 sets of muscle contractions:

The diaphragm contracts

Watch Video



http://www.interactive-biology.com/2659/062-pressure-changes-during-breathing/

http://www.interactive-biology.com/2659/062-pressure-changes-during-breathing/





The external intercostals contract.

Both of these will enlarge the volume of the thoracic cavity, which reduces the pressure in the pleural cavity, which means then that the pressure in the pulmonary cavity is greater than the pressure in the pleural cavity, forcing the lungs to expand.

Expiration - passive. The diaphragm relaxes, the external intercostals relax.When diaphragm contracts, this reduces abdominal cavity space, increasing the pressure in the abdominal cavity. When it relaxes, the abdominal organs push the diaphragm back into place. When thoracic cavity pressure goes up, pleural cavity pressure goes up above pulmonary pressure, and that forces air out.

Why don't the lungs collapse at the end of an expiration?The lungs are very elastic. This means that after we have expiratory movements, the lungs continue to become smaller. This reduces thoracic cavity pressure below atmospheric pressure. If the pressure in the thorax, and thus the pleural cavity, increases, this keeps the lungs from getting too small.Surfactant - released by special cells in the lungs that reduces surface tension of water. Part of the constriction of the lungs is the combined effect of surface tension and elasticity.

Dyspnea - forced breathing. The inspiratory phase is the same as Eupnea with two additional muscles connected to the clavicle (neck muscles).The expiratory phase is different. It involves the internal intercostals and the abdominal musculature. The internal intercostals pull the rib cage down. The abdominal muscle contract and force the diaphragm up by increasing abdominal pressure.

What happens if and of the walls of the thoracic cavity are penetrated?This is called a Pneumothorax, and that happens as a result of trauma. This means that the individual cannot breathe. When the diaphragm contracts, it simply sucks air though the hole in the wall. Fortunately, the 2 lungs are separate, so if only 1 lung collapse, you can use the other one. When you have a bilateral pneumothorax, breathing is no longer possible.







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