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Neuro anatomy Exam 1 > Phys Neuroplasticity > Flashcards

Phys Neuroplasticity Flashcards

1
Q

Axonal Injury (PNS):
4 Steps
(Discuss Wallerien Degeneration)

A
  1. Axon retracts away from post synaptic cell
  2. Wallerian Degeneration - myelin sheath gets peeled away and axon retracts further
  3. Glial cells/macrophages come in and eat up debris to prep area for axon to regrow
  4. Schwann cells guide axon to appropriate target
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2
Q

Axonal Sprouting:
Collateral -
Regenerative -

A

Collateral - new branches formed from neighboring cells
Regenerative - damaged axon regrows itself
(In adults, growth is slow and not precise)

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3
Q 
Axonal Injury (Central CNS):
2 Causes
A

Causes:
1. Decreased Blood Flow (Ischemia)
2. Neurodegenerative Disease (MS, PD)
(CNS axons typically do not re-grow after injury)

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4
Q

Why doesn’t CNS regenerate?

CNS damage triggers…

A
  1. CNS damage triggers necrosis (cell death directly related to injury) and apoptotic cell death (secrete chemicals that kill healthy neighbor neurons) of severed axons.
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5
Q

Why doesn’t CNS regenerate?

Clean-up…

A
  1. Clean-up is slow:
    - Lack of Schwann Cell Guidance
    - Lack of Macrophages
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6
Q

Why doesn’t CNS regenerate?
CNS environment is hostile to regenerative attempts:
Astrocytes -
Microglial Activation -

A

Astrocytes - when healthy, secrete proteins for health and homeostasis
- Glial scarring -> come to area of injury and form a scar that stops physically and chemically downstream effect of chemical death (stop further infections, stimulate revascularization, will stop growth)
Microglial activation - when healthy, immune cell that helps with tissue homeostasis
- Problem -> can’t distinguish between debris and other supportive structures and difficult to control

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7
Q

Neurogenesis -

A
  • Low level of GLIAL cells that can proliferate throughout our lifetime, except in two areas of brain:
    1. Olfactory bulb (smelling)
    2. Hippocampus (memory/learning)
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8
Q

What is neuroplasticity?

How can it be activated?

A
  • Ability of nervous system to respond to intrinsic stimuli by reorganizing its structure, function, and connections
  • Can occur during development, in response to environment, in support of learning, in response to disease, or in relation to therapy
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9
Q

Neuroplasticity Mechanisms:

Chemical

A

Chemical - brain increase NT it releases -> activate new postsynaptic receptors

  • Can occur quickly
  • Short term memory unless add additional support
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10
Q

Neuroplasticity Mechanisms:

Structural

A

Structural - Sustained changes can cause changes in axons

  • Takes more time
  • More long lasting (long term retention of new ability)
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11
Q

Neuroplasticity Mechanisms:

Functional

A

Functional - neurons can completely adopt new functions/roles when stimulated in specific way
(How we can survive neuro injury and how we see improvements)

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12
Q

Cortical Remapping:
Synaptic Pruning
(Examples)

A

-Example of functional neuroplasticity
Synaptic Pruning - eliminates/changes synapses based on what brain is being taught
Ex: Blindness - amount brain controls hand increases because necessary to read brail and increased senses to brain to compensate
EX: Phantom Limb - sensory aspects spill over into regions

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13
Q

Habituation -

What is it?

A
  • Simplest form of neuroplasticity
  • decrease response to repeated, benign stimulus (acclimation to light until you can tolerate)
  • Allow’s us to pay attention to what’s important (tune out white noise)
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14
Q

Short term vs Long term Habituation

A

Short term = <30 min
-Presynaptic in nature -> dump less NT -> blunts AP
-After stimulus is over-> changes will go away
Long term = >30 min
-Changes in postsynaptic -> receptors and proteins that sustain AP
-Long lasting structural changes

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15
Q

Clinical Applications of Habituation:

A

EX: Peds - child doesn’t like hot/cold, so repeat stimulus and gradually increase and child will become less sensitive
EX: Vestibular dysfunction - dizzy/unsteady when turn head, so repeat exposure to head turn and slowly increase gradually and it will decrease sensitivity

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16
Q

Learning and Memory:

Experience-Dependent Plasticity -

A
  • CNS uses experiences and modifies synaptic connections by increasing some while weakening others
  • After injury -> brain will attempt to restructure
  • More complex than habituation
17
Q

Long-term potentiation (LTP) -
What is it?
What type of intensity required?

A
  • Process by which the synaptic connections between neurons become stronger by frequent activation
  • Requires high intensity stimulation
18
Q 
LTP:
Low intensity exposure - 
Discuss mechanism (what receptors and what ions)
Is there structural change?
A
  • Few NT into synaptic cleft
  • Glutamate binds to NMDA and AMPA receptors - > open post synaptic membrane
    AMPA - Na+ flood into negative post synaptic cleft
    NMDA - Some Na+/mostly Ca++, however Mg blockade
  • Receptors stay open as long as there is glutamate
  • No structural changes
19
Q

LTP:
High intensity exposure -
Discuss mechanism
Coincidence receptors -

A
  • Increase glutamate release into synaptic cleft so receptors stay open longer
    AMPA - increase Na+ into post synaptic cell
    NMDA - electrostatic repulsion repels Mg+ blockade because of Na+ increase in post synaptic cell -> Ca++ enters cell
    -Coincidence Receptors - both presynaptic increase of AP frequency and post synaptic electrostatic repulsion need to occur for it to become functional
20
Q 
Role of Calcium in high intensity exposure 
(3)
1. Secondary messenger
2. Increase strength
3. Increase growth
A
  1. Influx Ca++ acts as secondary messenger -> activates secondary cascade that initiates structural changes for long term effect
  2. Increase strength: activates increase AMPA receptors for future depolarization (more sensitive to glutamate and increases response)
  3. Increase growth: increase growth factors (proteins) that are involved in growth of new synapses
21
Q

Long Term Depression -
What is it?
How does it stop long term potentiation and weaken activation?

A
  • Conversion of active synapses into silent ones
  • “Reset” button
  • Low intensity, prolonged stimulation -> not enough to removed Mg blockade (so no LTP) and will remove AMPA receptors from post synaptic cell (weakens activation)
22
Q

4 Ways you can use for Rehabilitation and Neuroplasticity:

A
  1. Technology
  2. Pharmacology
  3. Physical Rehab
  4. Cognitive Training
23
Q

Ten Principles of Neuroplasticity: (1-5)

A
  1. Use it or lose it
  2. Use it and improve it
  3. Specificity matters (interventions specific to goal)
  4. Repetition matters
  5. Intensity matters
24
Q

Ten Principles of Neuroplasticity: (6-10)

A
  1. Time matters (<6-12 months post injury ideal)
  2. Salience matters (should be important/meaningful)
  3. Age matters
  4. Transference or generalization (interventions cover many functions)
  5. Interference (start as soon as possible)

Neuro anatomy Exam 1 (13 decks)

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