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Receptors are transmembrane proteins that are either ion channels (nicotinic

receptors) or are coupled to intracellular second messengers (adrenergic &

muscarinic) that initiate the effect. When a specific neurotransmitter binds to its

receptor on a tissue, a response is elicited from the tissue that is characteristic of thereceptor-signaling cascade for that tissue.

At all autonomic ganglia presynaptic nerve endings release ACh which acts on

nicotinic (N2 or NN) receptors on the postganglionic nerve cell body

Postganglionic sympathetic axons release norepinephrine which acts on of three

receptors: , 1, 2 depending upon the end-organ

Postganglionic parasympathetic axons release ACh which acts on one of five

muscarinic receptors

Somatic motor axons release ACh which acts on a different type of nicotinic receptor

(N1 or NM)

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The postganglionic nerve endings of parasympathetic and sympathetic nerves can

end near one another on the same tissue. Because of this, transmitter released from

one type of nerve ending can affect transmitter release from the other.

NE released from sympathetic nerves can inhibit ACh release from parasympathetic

nerve endings and vice versa.

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*** Notice that the diagram indicates that sympathetic nerves decrease salivation.

This is incorrect. Salivation is increased by BOTH sympathetic and parasympathetic

nerves.

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The adrenergic and muscarinic receptors are G-protein linked receptors.

The alpha subunit of the G-protein is designated s, i or q.

In the case of M2 receptors, some are mediated by the direct action of the G-protein

subunit.

The nicotinic receptors are ligand-gated ion channels.

PLC = phospholipase C

AC = adenylyl cyclase

IP3 = inositol tris-phosphate

cAMP = cyclic adenosine monophosphate

If= funny channels that conduct Na

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The wall of the urinary bladder is composed primarily of smooth muscle called the detrusormuscle. Urine is prevented from leaving the bladder by preventing detrusor musclecontraction and keeping the internal and external sphincters closed.

There are stretch receptors located within the walls of the bladder that sense bladderfullness. When bladder volume begins to exceed 100 150 mls the stretch receptors initiatethe micturition reflex. The reflex is a spinal reflex that is modified by higher brain centers.This means that the reflex will occur even if the spinal cord is cut preventing input from thebrain.

When the stretch receptors signal bladder fullness, the activity of the somatic motor nerve(pudendal nerve) is inhibited allowing the external sphincter to open; simultaneously, theinternal sphincter also relaxes through stimulation of the parasympathetic nerves (ACh,muscarinic receptors) and inhibition of sympathetic nerves. The detrusor muscle contractsdue to parasympathetic stimulation and sympathetic inhibition.

After the bladder has emptied and the stretch receptors are no longer stimulated,

parasympathetic nerve activity diminishes and sympathetic nerve activity increases(norepinephrine, 2 receptor). This causes the detrusor muscle to relax and the internalsphincter to close (norepinephrine, 1 receptors) enabling filling. In addition, pudendalnerve activity increases closing the external sphincter (ACh, nicotinic N1).

After the age of 2-years-old higher brain centers have developed and inhibit the micturitionreflex so that voiding is under voluntary control and occurs at appropriate times. Thisinhibition of the reflex allows the bladder to fill to a larger volume until the appropriate timefor voiding.

If the spinal cord is severed above L1 the input from higher centers is eliminated and themicturition reflex is no longer inhibited. This results in lower bladder capacity, frequentvoiding and loss of voluntary control.