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Terms in this set (54)
ability of neurons to change their function, chemical profile (amount and types of neurotransmitters produced), or structure
neuroplasticity: positive or negative
- chronic pain
General term used to encompass the following mechanisms:
• Experience-dependent plasticity: learning and memory
• Cellular recovery after injury (or maladaptation)
a decrease in response to a repeated, benign stimulus
• One of the simplest forms of neuroplasticity.
• Cellular mechanisms responsible for habituation are not completely understood.
(last <30 minutes): presynaptic; decrease in release of excitatory neurotransmitter • Ex: Perfume, Watch
structural changes in a neuron and decrease in number of synapses
• Examples: PT vestibular rx; PT for children with tactile defensiveness
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING
Is a complex process involving persistent, long-lasting changes in the strength of synapses between neurons and in neural networks.
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING -- during initial phases of motor learning
initial phases of motor learning, large and diffuse regions of the brain are active.
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING---- task are repeated
tasks are repeated, the number of active regions in the brain are reduced.
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING----when motor task is learned
motor task is learned, only small, distinct regions of the brain show an increased activity when performing the task.
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING---requires
synthesis of new proteins, growth of new synapses, and/or modification or inhibition of existing synapses
EXPERIENCE DEPENDENT PLASTICITY: MEMORY AND LEARNING---mechanicisms
depend on the type of synapse and location involved:
• Plasticity of the excitability of neurons by functional changes of ion channels
• Plasticity at inhibitory GABAergic synapses
• Homeostatic plasticity to stabilize neural circuits
• Long-term potentiation (LTP)
• Long-term depression (LTD)
LONG TERM POTENTIATION AND DEPRESSION (LTP & LTD)
2 main types of plasicitiy in learn & memory fxn
LTP & LDP of
excitatory glutamatergic synapses
Strengthens connection between pre and post synaptic membranes.
-Repeated stim converts into greater post-synaptic potential.
----This makes better at opening channel to let more ions in.
effective for wk or months
HOW LTP HAPPENS
"silent" synapses are converted to active synapses
AMPA and NMDA receptors are involved:
Mobile APMA receptors get inserted into the membrane. Increased AMPA helps depolarization of neuron, which in turn aids opening of the NMDA receptors (which are blocked with magnesium)
LTD is opposite
TRANSCRANIAL MAGNETIC STIMULATION
Either enhances or inhibits motor learning/ formation
--depending on the frequency & experimental protocol used.
Magnetic stimulation of the brain is thought to induce
synaptic plasticity via LTP- or LTD-type mechanisms.
ASTROCYTES CONTRIBUTE TO EXPERIENCE DEPENDENT PLASTICITY
Release of a neurotransmitter by the neuron stimulates the release of gliotransmitters by the astrocyte.
neuronal activity & synpatic transmission
Influence synaptic plasticity through modulating neurotransmitter release
and receptor expression at the postsynaptic membrane.
ASTROCYTES CONTRIBUTE TO EXPERIENCE DEPENDENT PLASTICITY: may also be important for
new synapse formation following stroke
AXONAL INJURY IN THE PERIPHERY: growth
Growth of a new branch of intact axon or regrowth of damaged axons
denervated target is reinnervated by branches of intact axons of neighboring neurons
when axon and target cell have been damaged. Injured axon send out side sprouts to a new target.
AXONAL INJURY IN THE PERIPHERY: occurs more frequently in
PNS than CNS due to production of Nerve Growth Factor (NGF) by Schwann cells, effective cleaning of debris, and formation of bands of Bunger to guide axonal growth to the target
AXONAL INJURY IN THE PERIPHERY: exercise
5 days after peripheral nerve injury increases axonal regeneration
AXONAL INJURY IN THE CNS:
same processes that follow a peripheral axonal injury also occur following CNS injury (spinal cord injury, TBI, etc.)
AXONAL INJURY IN THE CNS: damage
evolves hours and days following the initial injury due to a cascade of cellular events.
AXONAL INJURY IN THE CNS: deficits
deficits depends on the degree of damage to white fiber tracts
AXONAL INJURY IN THE CNS: functional axon
Functional axon regeneration does not occur
AXONAL INJURY: injury that damage or sever axons cause
cause degeneration but may not result in cell death; some neurons have the ability to regenerate the axon.
AXONAL INJURY: that destorys the cell body leads to
death of cell
AXONAL INJURY: neuron dies, what happens
-nervous system promotes recovery by altering specific synapses
---> functionally reorganizing the CNS,
---> changing NT release in response to neural activity.
SYNAPTIC CHANGES FOLLOWING INJURY: Denervation hypersensitivity
occurs if presynaptic axons terminals are destroyed and new receptor sites develop on the postsynaptic membrane in response to decreased NT release.
SYNAPTIC CHANGES FOLLOWING INJURY: Synaptic hypereffectiveness
occurs when only some branches of a presynaptic axon are destroyed.
--->Causes remaining axon branches to release larger than normal amounts of NT
SYNAPTIC CHANGES FOLLOWING INJURY: Unmasking of silent synapses
unused synapses suddenly become active
FUNCTIONAL REORGANIZATION OF THE CEREBRAL CORTEX: adult brain
cortical areas routinely adjust way they process new info
FUNCTIONAL REORGANIZATION OF THE CEREBRAL CORTEX: cortical map
be modified by sensory input, experience, learning, and brain injury.
Cortical plasticity and reorganization are
likely mechanisms driving functional recovery after a stroke; reorganization can take years (2 years).
Reorganization after a nerve injury may be a factor in
some chronic pain
ACTIVITY-RELATED CHANGESIN NEUROTRANSMITTER RELEASE: repeated stimulation of somatosensory pathways can cause
increases in inhibitory neurotransmitters, decreasing the sensory cortex response to overstimulation.
ACTIVITY-RELATED CHANGESIN NEUROTRANSMITTER RELEASE: understimulation somatosensory pathways can cause
opposite effect, causing the cortex to be more responsive to weak sensory inputs
involved in brain remodeling following a neurological injury.
NEUROGENESIS: neural precursor cells
migrate toward the ischemic area after a stroke; many cells that arrive near the ischemic area do not survive, possibly as a result of inflammation
METABOLIC EFFECTS OF BRAIN INJURY: after stroke or brain injury
beyond cell death from lack of oxygen, excitotoxicity adds more damage
METABOLIC EFFECTS OF BRAIN INJURY: oxygen deprived
neurons release large amounts of glutamate
METABOLIC EFFECTS OF BRAIN INJURY: excessive levels glutamate
is toxic to neurons
• Binds persistently to NMDA receptors and causes a cascade of events which break down neurons and cause cell death
METABOLIC EFFECTS OF BRAIN INJURY: neuroprotective drugs
---block NMDA receptors (which blocks normal activity)
EFFECTS OF REHABILITATION ON PLASTICITY
TAKE HOME MESSAGES FOR PT
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