Neuroplasticity (unit 1)

what is neuroplasticity

- ability of neurons to change their function, chemical profile (amount and types of neurotransmitters produced), or structure

what is habituation

- a decrease in response to a repeated, benign stimulus

what is short term habituation

- lasts < 30 minutes and due to presynaptic changes

what is long term habituation

- prolonged repetition of stimulus and changes in post synaptic receptors

what is experience dependent plasticity

- complex process involving persistent, long-lasting changes in the strength of synapses between neurons and in neural networks

experience dependent plasticity requires

- synthesis of new proteins

- growth of new synapses

- modification of existing synapses

what happens in the initial phase of motor learning in experience dependent plasticity

- large and diffuse regions of the brain active

what happens when tasks are repeated during experience dependent plasticity

- number of active regions in the brain are reduced

what happens when a motor task is learned during experience dependent plasticity

- small, distinct regions of the brain show an increased activity

what is long term potentiation (LTP)

- silent synapses -> active

- glutamate binds to NMDA receptor (activating it to allow cations to cross)

> increased Ca2+ causes mobile AMPA receptors to be inserted into membrane

what is long term depression (LTD)

- active synapses -> silent

- AMPA receptors removed from membrane

- post synaptic membrane less likely to depolarize when glutamate is released into cleft

what is transcranial magnetic stimulation

- either enhances or inhibits motor learning and memory formation, depending on the frequency and experimental protocol

what is astrocytic contribution

- communication between astrocytes and neurons occur via the release of a neurotransmitter by the neuron (stimulates the release of gliotransmitters by the astrocyte)

- influence synaptic plasticity through modulating NT release and receptor expression at the postsynaptic membrane

what are gliotransmitters

- modulate neuronal activity and synaptic transmission

what happens when oxygen deprivation post CVA or TBI

- neurons die and do not regenerate

what happens with excitotoxicity

- oxygen deprived neurons release excess glutamate

- high concentration of glutamate kills post synaptic neurons

what happens with an axonal injury

- splits into 2 segments:

- proximal segment (connected to cell body)

- distal segment (part isolated from soma)

- immediately after injury, cytoplasm leaks out and segments retract

- distal part undergoes wallerian degeneration

axonal injury - distal part (which is isolated from the soma undergoes Wallerian Degeneration)

1. myelin sheath pulls away

2. axon swells and breaks into shorter segments

3. terminals rapidly degenerate and their loss is followed by death of the entire distal segment

4. glial cells clean up debris

5. soma undergoes central chromatolysis (degenerative changes)

what type of injuries occur in the PNS

- severance injuries

- injuries from sharp objects or by extreme stretch that pulls axon apart

what is sprouting

- growth of new branch of an intact axon or regrowth of damaged axon

what is collateral sprouting

- denervated target reinnervated by neighboring neurons

what is regenerative sprouting

- when axon and its target cell have been damaged and injured axon sends out side sprouts to a new target

what is diffuse axonal injury

- inertial force cause widespread tearing and stretching of axons

- causes widespread disconnections between neurons

- devastating functional deficits

in summary both PNS and CNS go through

- axonal retraction

- wallerian degeneration

- central chromatolysis

functional regeneration

- PNS has function regeneration (collateral and regenerative sprouting)

- CNS does not have functional regeneration

cellular recovery from injury

- injuries that damage or sever axons cause degeneration but may not result in cell death

nervous system promotes recovery by?

- altering specific synapses

- reorganizing the CNS

- changing NT release

what are the synaptic mechanisms

1. recovery of synaptic effectiveness

2. denervation hypersensitvity

3. synaptic hyper effectiveness

4. unmasking of silent synapses

functional reorganization of the cerebral cortex

- cortical areas routinely adjust the way they process info

- they also retain ability to develop new functions

- changes at individual synapses reorganize the brain (leading to functional changes)

cortical maps can be modified by?

- sensory input

- experience (practicing a certain skill)

- learning

- peripheral or brain injury

activity related changes in neurotransmitter release

- repeated stimulation of somatosensory pathways can cause increases in inhibitory NT

> decrease the sensory cortex in response to overstimulation -> habituation

- understimulation can have the opposite effect

> cortex to be more responsive to weak sensory inputs

what is neurogenesis

- stem cells are involved in brain remodeling following a neurological injury

- neural precursor cells migrate toward the ischemic area after a stroke

> many cells that arrive near the ischemic area do not survive, possibly a result of inflammation

effects of rehab on plasticity

- plasticity allows for recover post insult

- active movement (crucial for optimizing motor recovery)

- intensity

- early initiation (critical for recovery)

task specific training in chronic phase post CVA

- produces long lasting cortical reorganization in the brain areas activated

> induces more regular patterns of brain activation

constraint induced movement (CIMT) training in chronic phase post CVA

- induces functional reorganization of the cortex in individuals post CVA

Kleim & Jones Principles of Neuroplasticity

1. use it or lose it (neural pathways will die if not used)

2. use it and improve it (extended training)

3. specificity (how you train= specific to what you want to improve)

4. repetition (practice)

5. intensity (low intensity=less response, high intensity=high response)

6. time (the time when you do it matters)

7. salience (tasks you're attentive to, make the task important)

8. age (younger kids can have greater neuroplasticity than adults)

9. transference (training under one context might help you in another context)

10. interference (outside stimulations can interfere with learning)

use it or lose it

- neural circuits not actively engaged for an extended period of time, degrade. Failure to engage a brain system due to lack of use may lead to further degradation of function

use it and improve it

- plasticity can be induced in specific areas of the brain with extended training. PERMANENT changes in CNS can be induced through extensive training.

Specificity

- training in specific modality may change part of the neural circuitry involved in more general function and thus positively impact the potential for learning in non-trained activities. Learning, or skill acquisition, rather than mere use, is required to produce significant changes in neural connectivity.

repetition

- repetition of newly learned skill is necessary to induce lasting changes

intensity

- low-intensity repetition can induce a weakened response, whereas higher stimulation will produce long-term changes. Must modify to match changing skill level of patient.

time

- there may be windows of time during which the learning is most effective after BI. In general, training soon after injury is most effective.

salience

- tasks that have meaning to the learner promote learning. Functionally relevant.

age

- younger brains respond to experience differently than aging brains. There is evidence of neuronal sprouting earlier & smaller sized lesions in younger brains. Aging brain is responsive to experience, but changes less profound & are slower.

transference

- exercise results in angiogenesis in motor cortex, providing fertile ground to support learning. Fertile ground for more learning. Plasticity in response to one training experience can enhance acquisition of similar behaviors (ie. Transfers, walking in pool vs BWS vs over ground)

interfernce

- stimulation applied outside of training may disrupt the memory consolidation process. Development of compensatory behaviors may interfere with learning optimal behaviors. Don't' be too quick to give AD.