Neuroplasticity

In the Soma, Neuroplasticity normally takes to form of

1. Altered gene expression a. This may lead to altered protein synthesis b. Alterations in cell health or function.

At the synapse, plasticity can take the following forms

1. Increased/Decreased number of synaptic vesicles in the presynaptic terminal. 2. Increased/Decreased number/density of postsynaptic membrane receptors 3. A change in the type of postsynaptic membrane receptor 4. Formation of novel synapses on the same cell (normally associate with dendritic spine changes) 5. Pruning of established synapses

In the axon, Neuroplasticity normally takes one of two forms

1. Regnerative sprouting (regeneration) (slide 7) a. The proximal end of severed axons may reform a growth cone and restart the process of axon elongation. In practice, this occurs in the PNS only 2. Collateral Sprouting a. An intact axon will sprout a collateral branch to synapse on neurons it did not previously synapse on.

Functionally, the plastic changes result in

1. The strengthening of connections between neurons. This can be thought of the strengthening of circuit 2. The weakening or loss of connections between neurons. This can be thought of the loss or weakening of a circuit 3. Novel connections between neurons that previously were not connected by a synapse. This can be thought of as the formation of novel circuits 4. Cells becoming healthier or taking on new functions. This can be thought of cellular survival and adaptation.

This special characteristic allows the brain's estimated 100 billion nerve cells, (neurons) to

constantly lay down new pathways for neural communication and to rearrange existing ones throughout life, thereby aiding the processes of learning, memory, and adaptation through experience.

It is involved in normal

development, learning, memory, and recovery from injury.

Without the ability to make such functional changes, our brains would not be able to

memorize a new fact or master a new skill, form a new memory or adjust to a new environment; we, as individuals, would not be able to recover from brain injuries or overcome cognitive disabilities.

Because of the brain's neuroplasticity,

old dogs, so to speak, regularly learn new tricks of every conceivable kind."

Neuroplasticity is driven by

the genetic code (nature), experience (nurture), and injury.

Hebb's Law or Hebbian Learning Rule

It states that "Cells that fire together, wire together". This basically means that the synapse of two neurons is strengthened when their temporal activation is concurrent.

Neuroplasticity

The ability of the CNS or neurons to change or retrain to change 1. Change their function, and/or 2. Change their chemical profile (amount and types of neurotransmitters and/or receptors), and/or 3. Change their structure (number and size of dendrites, soma size, axonal sprouting, and axonal regeneration)

Activity is

a major force in the promotion of neuroplasticity. A major tenet of neuroplasticity is Hebb's Law or Hebbian Learning Rule

4. Formation of novel synapses on the same cell (normally associate with dendritic spine changes)

a. Depending upon the type of receptors at these novel synapses, it could increase or alter the effects of a neurotransmitter on the postsynaptic neuron

3. A change in the type of postsynaptic membrane receptor

a. This will alter the postsynaptic neuronal responses to neurotransmitter release

2. Increased/Decreased number/density of postsynaptic membrane receptors

a. This will increase or decrease the response of the postsynaptic neuron to neurotransmitter release.

1. Increased/Decreased number of synaptic vesicles in the presynaptic terminal.

a. This will result in increased/decreased release of neurotransmitter in response to a single action potential, thereby possible increasing/decreasing the effects of that action potential.

5. Pruning of established synapses

a. Will decrease or eliminate the connection between the two neurons