Neuroplasticity Flashcards
what is neuroplasticity?
allows the NS to make changes in response to internal and external demands
what is neuroplasticity critical for?
learning, memory formation, and recovery from disease or injury
short term neuroplasticity changes
change in synaptic efficiency; chemical changes
long term neuroplasticity changes
synaptic/structural changes
what is habituation?
a decrease in synaptic activity w/repetitive stimuli
repeat synaptic activity b/w afferent efferent decreases
stimulus specific
what is the simplest form of neuroplasticity?
habituation
what is short term habituation?
immediately reversible after a few minutes
less calcium influx synaptically=less synaptic vesicles released
what is long term habituation?
structural changes:
- decrease # of synapses
- decrease post synaptic receptors through internalization and inactivation
what is sensitization?
increase in response to stimulus, specifically painful stimulus
non-noxious stimulus illicits pain
not stimulus specific
decreased w/drawal threshold-weaker stimuli can elicit the same response as stronger stimuli
what is central sensitization?
in the CNS
low threshold mechanoreceptors activate nociceptor
hyperalgesia and allodynia
what is hyperalgesia?
exasperated pain response
what is allodynia?
stimulus that shouldn’t hurt hurts
what is primary hyperalgesia?
increased pain sensitivity at the site of injury
decreased pain threshold and increased glutamate and substance P
what is secondary hyperalgesia?
sensitization outside the area of injury at the adjacent sites
what does experience dependent mean?
no exposure to experience=no plasticity in the brain
what are the biological changes required for memory and learning?
protein synthesis
modification of existing synapses
synaptogenesis (creation of new synapses)
what are dendritic spines?
projections from dendrites
common site for synaptic connections
what is long term potentiation?
activity dependent strengthening of synapses
silent–>active synapses
increased glutamate activates AMPA receptors which removes the magnesium block from NMDA receptors to allow more activity and more synaptic sites over time
increased presynaptic vesicles and increased receptors postsynaptically
need lots of repetition
what is long term depression?
activity dependent decrease in synaptic efficacy
weakened synaptic transmission b/w 2 neurons
active–>silent synapses
inactivity- of synapses=decreased AMPA receptors=less receptor activity
in cerebellum=learning new info
in hippocampus=loss of memory
what is the role of astrocytes in neuroplasticity?
astrocytes release gliotransmitters (like NTs)
moderates neural activity and synaptic transmission
- CNA modulate how much NT is released, expression of receptors in postsynaptic membrane, synaptogenesis, and Remodeling of axons after injury
linked to calcium
what are good plasticity changes?
learning
declarative memory (names, events-hippocampus)
procedural memory (motor acts-motor cortex)
recovery from CNS injury
what are the metabolic effects of neuronal injury in the CNS?
ischemia leads to glutamate release which leads to activation of calcium channels- and release of internal calcium stores
calcium release can lead ot 3 different things:
1. increased glycolysis bc sodium-potassium pumps are activated by the postivie charge which requires ATP form gylcolysis. Glycolysis creates excess lactic acid buildup that causes cell injury and feath
2. increased calcium leads to increased water in the cells leading to cell swelling and cytotoxic edema causing cell injury and death
3. increased calcium leads to activated protein enzymes (protease) which releases oxygen free radicals and causes cell injury and death
what is cytotoxic edema?
too much water intracellularly
what is wallerian degeneration?
CNS and PNS
occurs distal to the lesion
3-5 days in motor neurons; 6-10 days in sensory neurons
distal axon is broken down and eaten up by macrophages
chromatolysis: soma gets larger and nucleus moves peripherally
what occurs in the CNS after axonal injury?
no regeneration
denervation hypersensitivity: death of pre neuron, so post neuron inserts a lot of receptors that become very sensitive to stimuli
synaptic hypereffectiveness: from 3 pre to 1 pre that becomes hypereffective to make up for the loss
unmasking of silent synapses: silent synapses become active
what are the mechanisms of axonal recovery in the PNS?
collateral sprouting: pre neuron dies and remaining pre neuron takes on the orphan post neuron
- 1 to 2
regenerative sprouting: a post neuron dies to both pre go to one post neuron
- 2 to 1
regeneration in the PNS
axonal sprouting from the proximal axon
guidance from Schwann cells creating bands of Bunger that guide the spouts to target tissues
what is Bell’s Palsy?
axonal sprouting to the wrong target tissues
CN 7 injury
PNS axons go to wrong target
synkinesis: voluntary activation of one muscle leads to involuntary activation of another muscle
what is reorganization of the cerebral cortex?
region lost (amputation), representation in the homonculus decreases and other areas increase
larger on homonculus=more innervation=more fine motor control
what factors influence neuroplasticity?
neuronal activity (LTD and LTP)
growth factors: BDNF and NGF
- support survival and maintainance of neurons (increased by exercise)
what are the effects of rehab on neuroplasticity?
lack of movement=loss of function in areas adjacent to lesion
influenced by intensity, timing, and type of intervention
the earlier the better
