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Neuronal Plasticity
BySyed Mujtaba Hasnain Nadir
Mubarak Raza Wagha
What is neuronal plasticity?
Plasticity is the quality of being ‘plastic’ or formative.
Neuronal plasticity refers to the ability of the brain to change and adapt itself as a result of
one’s experience.
Applications of Neuronal Plasticity
• ‘Learning new things’• ‘Making new memories’• ‘Rewiring circuits’
Types of Long-term Memory
The NS is a series of connections
• Birth = 100 billion neurons
• 6 year old has twice as many synapses as an adult
• By late adolescence, synapses begin to disappear
http://www.eng.yale.edu/synapses.htm
Types of Neuroplasticity
Type Mechanism Duration
1. Enhancement of existing connectionsSynapse development Physiological ms-1 to hours
Synapse strengthening Biochemical hours to days
2. Formation of new connectionsUnmasking Physiological minutes to days
Sprouting Structural days to months
3. Formation of new cellsSelf-replication stem cell variable
Enhancement of existing connections
• Increased use of a synapse in existing pathways e.g. learning a new task
• Or alternative pathways following damage
• Cortical re-mapping (phantom limb)
Synapse development
Increased afferent input
New synapses evolve leading to increased excitation
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Synapse strengthening
Two point discrimination threshold in pianists index finger
R L
Ragert et al., 2004
Synaptic Strengthening
1. Facilitation (10-100 ms)
2. Augmentation (several seconds)
3. Potentiation (seconds to minutes)
Formation of new connections
• Unmasking of pre-existing pathways
• Sprouting of new pathways
Unmasking of silent synapses
Possible reasons why some synapses could be ‘silent’
• On distal dendrites• Inhibited by dominant pathways• Too little transmitter• Too few receptors• Don’t fire with other inputs
Unmasking – inhibition of subservient pathway by dominant pathway
+ +
Subservient pathway
Parallel pathway; neurons with a comparable role
Dominant pathway
Unmasking
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Lesion to dominant pathway
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Subservient pathway is unmasked
Activity is continued
despite lesion
Sprouting
Cell body
AxonAP
Sprouting
lesion
INJURY
Nerve Growth Factor (NGF)
Sprouting
lesion
INJURY
NGF
Neurite induced to sprout by NGF
Sprouting
Cell is re-innervated from alternative
stimulus
Sprouting may be a means of recovery; it may also produce unwanted effects
Injury results in cell death
Neurogenesis• Replacing dying or damaged
neural cells with new ones
• New cells originate from stem cells
• Introduced stem cells are stimulated to produce neural cells by nerve growth factors (NGF)
Stem cell/www.stanford.edu/group/hopes/rltdsci/nplast
Cortical Re-Mapping
• People born deaf
Cortical Re-Mapping
• People born deaf– What happens?
Cortical Re-Mapping
• People born deaf– What happens?
Visual areas increase in size and “jobs”
Cortical Re-Mapping
• People born deaf– What happens?
Visual areas increase in size and “jobs”Auditory areas may be “taken over” for visual
function
Cortical Re-Mapping
• People born deaf– What happens?
Visual areas increase in size and “jobs”Auditory areas may be “taken over” for visual
function Improved attention to movement in the periphery
The Basis of Neuronal Plasticity
Hebb’s Rule :
“Neurons that fire together, wire together.””Neurons that fire apart, wire apart.”
From The Organization of Behavior by Donald Hebb, 1949:
• "When one cell repeatedly assists in firing another, the axon of the first cell develops synaptic knobs (or enlarges them if they already exist) in contact with the soma of the second cell."
• Hebb postulated that this behavior of synapses in neuronal networks would permit the networks to store memories.
Synaptic Strengthening
1. Facilitation (10-100 ms)
2. Augmentation (several seconds)
3. Potentiation (seconds to minutes)
Long Term Potentiation
In neuroscience, long-term potentiation (LTP) is a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously.
Input specificity
• Once induced, LTP at one synapse does not spread to other synapses; rather LTP is input specific.
Cooperativity
• LTP can be induced by strong stimulation at one synapse
OR
• Weak stimulation at multiple synapses which together depolarize the post synaptic membrane to induce LTP
Hippocampus
Function:
• Consolidation of New Memories • Emotions• Navigation• Spatial Orientation
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
The post-synaptic region has both NMDA and AMPA receptors.
Glutamate first activates AMPA receptors. NMDA receptors do not respond until enough
AMPA receptors are stimulated and the neuron is partially depolarized.
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
NMDA receptors at rest have a magnesium ion (Mg2+) block on their calcium (Ca2+) channels.
After partial depolarization, the block is removed and the NMDA receptor allows Ca2+ to enter in response to glutamate.
Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 1)
Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 2)
Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 3)
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
The large Ca2+ influx activates certain protein kinases – enzymes that add phosphate groups to protein molecules.
One protein kinase is CaMKII – it affects AMPA receptors in several ways:
• Causes more AMPA receptors to be produced and inserted in the postsynaptic membrane.
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
CaMKII :• Moves existing nearby AMPA receptors into the active
synapse.• Increases conductance of Na+ and K+ ions in
membrane-bound receptors.These effects all increase the synaptic sensitivity to
glutamate.The activated protein kinases also trigger protein
synthesis
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
Strong stimulation of a postsynaptic cell releases a retrograde messenger that travels across the synapse and alters function in the presynaptic neuron.
More glutamate is released and the synapse is strengthened.
Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits
• Somatic intervention experiments – pharmacological treatments that block LTP impair learning.
• Behavioral intervention experiments – show that training an animal in a memory task can induce LTP.
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