Neuroplasticity L2

Bach-y-Rita, 1980 - Definition of Neuroplasticity

Neuroplasticity refers to the adaptive capacity of the central nervous system, that is, the ability to modify its own structural organisation and funcitoning

Nudo 2006 - Definition of Neuroplasticity

The capability of the cerebral cortex to alter its functional organisation as a result of experience

Examples of neuroplasticity in action

Chronic Experience

• Braille

• Musicians

• Athletes

• Taxi Drivers

• Interpretors

• Bilinguals

Rehabilitation

• learning to walk again after stroke

Mechanisms of Recovery with neuroplasticity

• Altering structure

• Altering Chemicals

• Altering Function

3 Elements of Altering Structure

• Unmasking

• Sprouting

• Vicariation of Function

Unmasking/The Redundacy Theory

Several synapses may mediate the same function in the brain, and some may be very active while others are redundant or ‘silent’

Unmasking is the phenomenon whereby silent synapses are facilitated to become the primary synapses of the damaged areas of the brain

Success depends on denervation supersensitivity, learning dependent synaptogenesis and long term potentiation

Sprouting and its 2 types

• Collateral Sprouting

• Regenerative Sprouting

Both act as a rewiring mechanism to allow lost function to be regained

It begins within 4-5 days of injury

Collateral sprouting seems more effective than regenerative, however without neurotransmitter influences leading to long term potentiation, a new pathway may not be established

Collateral Sprouting

The growth of sprouts from undamaged axons to form a connection with the damaged tissue

Regenerative Sprouting

The attempt of damaged axons to re-establish connection with the damaged tissue

Collateral vs Regenerative Sprouting

Collateral sprouting seems more effective than regenerative, however without neurotransmitter influences leading to long term potentiation, a new pathway may not be established

Vicariation of Function

How other cortical or subcortical structures, adjacent or remote from damaged area, are thought to take over or assume function of the damaged area

These areas may not have been directly involved with those functions before the injury

Mechanism of Recovery with altering chemicals

• Neurotransmitter regulation

• Denervation supersensitivity

Neurotransmitter regulation

Neurotransmitters

• Neuroplasticity depends on a balance of excitatory, inhibitory and modulatory signals. GABA prevents overactivity, while glutamate via NMDA receptors is crucial for long term potentiation and learning. BDNF acts as a brain fertiliser to support synapse growth and survival. Other neurotransmitters also fine tune plasticity

Environment

• Plasticity is also shaped by environment as enriched experiences like learning, excercise and social activity upregulate growth factors, signalling pathways and epigenetic changes, while downregulating processes limiting plasticity

Together neurotransmitters and environment enhance brain repair and protects against aging and disease.

Key neurotransmitters + factors involved in up-regulation

Experiences like learning, excercise and complex environments increase the release of the following:

• Growth factors like IGF-I and BDNF

• Signalling molecules like PKA, CREB, intracellular kinase

• Epigenetic modifications like histone acetylation which opens DNA for gene transcription

• Synaptic receptors like NMDA

• More NT release - eg Glutamate, serotonin, dopamine

• Neuronal adhesion molecules help stabilise new connections

Key NTs and factors in down-regulation

• DNA methylation - gene silencing

• Too much inhibition or excitation

• Extracellular matrix components, which limit plasticity if overexpressed

• Beta - amyloid, which is toxic in Alzheimer’s, and linked to impaired plasticity

The effects of up regulation dominance

• enhanced plasticity

• Faster brain development in children

• Brain repair after injury

• Rescue of intellectual disability phenotypes (improve function of the intellectually disabled)

• Improved brain health during aging

Denervation Supersensitivity

As a result of partial denervation of neurons, post synaptic neurons can become more responsive to the neurotransmitters of the remaining affects, which may have positive or negative effects.

It increases existing synapses effectiveness and allows recovery to occur

The 4 Key Factors for the recovery of function

LDS, LTP, SI, AMN

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• Learning Dependant Synaptogenisis

• Long Term Potentiation

• Sensory Intergration

• Avoidance of Maladaptive Neuroplasticity

Learning Dependent Synaptogenesis

The formation of new synapses through an increase in dendritic branching and spine density, no.of synapses per neuron, and no.of synapses with synaptic boutons.

• this can only occur once the axon has reached its destination and is therefore dependent on sprouting and denervation supersensitivity

Hebb’s Rule

“Learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active, due to task repetition”

Long Term Potentiation

A persistent strengthening of synapses based on recent patterns of behaviour