Neuroplasticity

Question 1

what is neuroplasticity?

Answer 1

allows the NS to make changes in response to internal and external demands

Question 2

what is neuroplasticity critical for?

Answer 2

learning, memory formation, and recovery from disease or injury

Question 3

short term neuroplasticity changes

Answer 3

change in synaptic efficiency; chemical changes

Question 4

long term neuroplasticity changes

Answer 4

synaptic/structural changes

Question 5

what is habituation?

Answer 5

a decrease in synaptic activity w/repetitive stimuli

repeat synaptic activity b/w afferent efferent decreases

stimulus specific

Question 6

what is the simplest form of neuroplasticity?

Answer 6

habituation

Question 7

what is short term habituation?

Answer 7

immediately reversible after a few minutes

less calcium influx synaptically=less synaptic vesicles released

Question 8

what is long term habituation?

Answer 8

structural changes:
- decrease # of synapses
- decrease post synaptic receptors through internalization and inactivation

Question 9

what is sensitization?

Answer 9

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

Question 10

what is central sensitization?

Answer 10

in the CNS

low threshold mechanoreceptors activate nociceptor

hyperalgesia and allodynia

Question 11

what is hyperalgesia?

Answer 11

exasperated pain response

Question 12

what is allodynia?

Answer 12

stimulus that shouldn’t hurt hurts

Question 13

what is primary hyperalgesia?

Answer 13

increased pain sensitivity at the site of injury

decreased pain threshold and increased glutamate and substance P

Question 14

what is secondary hyperalgesia?

Answer 14

sensitization outside the area of injury at the adjacent sites

Question 15

what does experience dependent mean?

Answer 15

no exposure to experience=no plasticity in the brain

Question 16

what are the biological changes required for memory and learning?

Answer 16

protein synthesis

modification of existing synapses

synaptogenesis (creation of new synapses)

Question 17

what are dendritic spines?

Answer 17

projections from dendrites

common site for synaptic connections

Question 18

what is long term potentiation?

Answer 18

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

Question 19

what is long term depression?

Answer 19

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

Question 20

what is the role of astrocytes in neuroplasticity?

Answer 20

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

Question 21

what are good plasticity changes?

Answer 21

learning

declarative memory (names, events-hippocampus)

procedural memory (motor acts-motor cortex)

recovery from CNS injury

Question 22

what are the metabolic effects of neuronal injury in the CNS?

Answer 22

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

Question 23

what is cytotoxic edema?

Answer 23

too much water intracellularly

Question 24

what is wallerian degeneration?

Answer 24

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

Question 25

what occurs in the CNS after axonal injury?

Answer 25

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

Question 26

what are the mechanisms of axonal recovery in the PNS?

Answer 26

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

Question 27

regeneration in the PNS

Answer 27

axonal sprouting from the proximal axon

guidance from Schwann cells creating bands of Bunger that guide the spouts to target tissues

Question 28

what is Bell’s Palsy?

Answer 28

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

Question 29

what is reorganization of the cerebral cortex?

Answer 29

region lost (amputation), representation in the homonculus decreases and other areas increase

larger on homonculus=more innervation=more fine motor control

Question 30

what factors influence neuroplasticity?

Answer 30

neuronal activity (LTD and LTP)

growth factors: BDNF and NGF
- support survival and maintainance of neurons (increased by exercise)

Question 31

what are the effects of rehab on neuroplasticity?

Answer 31

lack of movement=loss of function in areas adjacent to lesion

influenced by intensity, timing, and type of intervention

the earlier the better