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Neuro COPY > Neuroplasticity > Flashcards

Neuroplasticity Flashcards

1
Q

What are some causes of axonal injuries in the PNS

A

stretch
crush
shear
laceration

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2
Q

What are the 3 types axonal injuries in the PNS from least severe to most severe

A

neuropraxia
axonotmesis
neurotmesis

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3
Q

neuropraxia

A

local myelin damage, axon stays intact
sx: weakness, numb, tingling, hyposensitivity
AP slowed down

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4
Q

axonotmesis

A

continuity of axon lost leads to Wellerian degeneration

may or may not include damage to epineurium, perineurium, and endoneurium

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5
Q

what is Wallerian degeneration

A

axon degeneration that occurs after a PNS axonal injury

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6
Q

neurotmesis

A

complete transection of a nerve and it is unable to grow back
surgery is necessary
still see Wallerian degeneration

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7
Q

What are the 6 cellular events after a peripheral n injury

A
  1. Wallerian degeneration (distal to injury)
  2. Macrophages clear debris and Schwann cells become phagocytic and engulf degenerating axon and myelin
  3. center end of axon (proximal) sprouts into endometrial sheaths left behind by degenerated axon
  4. Schwann cells proliferate as axon regrows
    • prod of new myelin
    • guide axon regrowth
  5. axon re-establishes postsynaptic target (where we see pts improve)
  6. axon diameter increases, more myelin created with time
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8
Q

When peripheral axons get injured they degenerate ______ to _____

A

distal to proximal

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9
Q

how many mm/day and cm/wk do peripheral axons regrow

A

1

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10
Q

what is collateral sprouting

A

neighboring PNS neuron sprouts from own neuron to communicate with the postsynaptic target that the injured neuron used to communicate with

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11
Q

regenerative sprouting

A

axon is able to regrow but changes its postsynaptic target

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12
Q

what are the 3 causes of CNS axonal injuries

A

trauma
decreased blood flow (ischemia)
neurodegenerative disease

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13
Q

what is the bad news about CNS axonal injuries

A

axons typically do not regrow after injury

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14
Q

what is the good news about CNS axonal injuries

A

out brain can create new pathways to compensate for axons lost
we only use about 10% of brain until something goes wrong

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15
Q

What are some causes for the CNS to not be able to regenerate?

A

CNS damage triggers necrosis and apoptotic cell death of severed axons
slow cleanup
hostile environment in regenerative events

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16
Q

What happens when necrosis and apoptotic cell death occurs

A

when the brain causes this the damaged cells release neurotoxins into brain and they travel to healthy tissues and kill them too

17
Q

what causes the hostile environment in CNS

A 
astrocytes - glial scarring (these can block any attempt on axon regrowing)
microglial activation (clear away debris but cannot distinguish bw good and bad)
18
Q

What are two areas believed to show potential for neurogenesis in CNS and what kind of cells are going to be able to do this

A

olfactory bulb
hippocampus
glial cells NOT neuronal cells

19
Q

what is neuroplasticity

A

the ability for the NS to respond to intrinsic stimuli by reorganizing its structure, function, and connections
can occur in development, response to environment, learning, disease, or therapy

20
Q

what are the 3 things that activate neuroplasticity

A

environmental
behavioral
neural processes

21
Q

what are the five neuroplasticity mechanisms

A 
chemical
structural
functional
habituation
LT Potentiation and Depression
22
Q

what is chemical neuroplasticity

A

immediate to ST changes to chemical synapses
increase NT released in synaptic cleft
happens when start using a new pathway repetitively

23
Q

what is structural neuroplasticity

A 
LT changes to neuronal structure
modify existing postsynaptic receptors
create new postsynaptic receptors
increased dendritic and terminal axonal growth
creates a stronger pathway
24
Q

what is functional neuroplasticity

A

LT changes to neuronal function
neurons change roles, function, and info relayed
this is how we recover from an injury

25
Q

cortical remapping

A

process in which the cortical map is affected and changed by sitimulus

26
Q

what is the earliest occurrence of cortical remapping

A

infancy

synaptic pruning

27
Q

what are some examples of cortical remapping in adults

A

blindness - we heighten other senses esp hand function/sensation to read braille
phantom limb - cortical does not understand why limb is not there but eventually realizes

28
Q

habituation

A 
decreased response to a repeated, benign stimulus
ST < 30 min - change presynaptically
  - decease excitatory release of NT
LT > 30 min - change postsynaptically
   - decrease receptors
29
Q

experience-dependent neuroplasticity

A

selective stabilization of certain synapses and removal of others in response to experience
more complex than habituation
manifested through LT potentiation and depression

30
Q

LT potentiation (LTP)

A

process by which the synaptic connections bw neurons become stronger by frequent activation
require high intensity stimulation

31
Q

LTP has two types of postsynaptic receipts and what do they include

A

AMPA receptors
- permeable to Na
- ligand receptors, open in response to glutamate linking
NMDA receptor
- permeable to Na and Ca
- contain Mg blockade to make it more picky what goes through

32
Q

LTP NMDA receptors require what to happen

A

pre and postsynaptic events to happen
need rapid fire of AP
“coincidence receptors”

33
Q

What is the role of Ca in LTP

A

secondary messenger than activate secondary intracellular cascade in postysnpatic for structural changes
increase post AMPA receptors - more ready to accept glutamate
increase growth factors - new synapses

34
Q

what is LT depression (LTD)

A

conversion of active synapses into silent ones
helps “clear the slate”
low-intensity, prolonged stimulation

35
Q

how is pharmacology involved in rehab and neuroplasticity

A

fluoxetine is an antidepressant that facilitates neuroplasticity after brain injury/stroke

36
Q

who has the biggest clout in rehab and neuroplasticity

A

physical rehabiliation

Neuro COPY (4 decks)

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