Ch. 4: Neuroplasticity

Question 1

Signs/Sx of Nerve Irritation

Answer 1

Tingling

Question 2

Signs/Sx of Asleep Nerve

Answer 2

Sensation/Motor Loss

Question 3

Signs/Sx of Nerve Death

Answer 3

Sensation/Motor Loss

Question 4

Wallerian Effect

Answer 4

Distal to axon injury

Question 5

Habituation

Answer 5

• decrease strength of synaptic connections (like down regulation)
• Short-lived decrease in strength of response following repeated benign stimulation
• May be due to decrease release of excitatory neurotransmitters

Question 6

Adaptation

Answer 6

-Structural changes due to long term habituation

Question 7

LTP

Answer 7

• Long term potentiation
• Persistent, long lasting changes in strength of synaptic connections

-AKA: experience-dependent plasticity

Question 8

Conversion of Silent Synapses to Active Synapses

Answer 8

• AMPA Receptors inside post synaptic cell get pushed to the membrane for use when Calcium enters the cell though other (NMDA) receptors when glutamate binds to it
• with stimulation: post synaptic cell creates another dentritic spine with clusters of receptors and presynaptic membrane changes shape too

Question 9

Types of Sprouting

Answer 9

• Regenerative

- Collateral

Question 10

Regenerative Sprouting

Answer 10

-Damaged neuron regrows axon if soma still alive

Question 11

Retrograde Effect

Answer 11

-Proximal to axon injury

Question 12

Stroke (FAST)

Answer 12

F-facial droop
A-arm weakness
S-slurred speech
T-time

Question 13

Recovery of synaptic effectiveness

Answer 13

• Resolution of swelling–>axon wakes up

- “shadow of death” recovers and regains blood supply

Question 14

Collateral Sprouting

Answer 14

• if soma dies after injury a surviving neuron sends out a branch to the target cell
• Collaterals can fail over time

Question 15

Axonal Injury in CNS

Answer 15

Doesn’t sprout collaterals or regenerate

Question 16

CNS MOI

Answer 16

• Mechanical (tear, shear, projectile)

- Chemical (ischemia, excitotoxicity)

Question 17

Synaptic Hypereffectiveness

Answer 17

• Divergent nerve partially damaged but still produce same amount of neurotransmitters
• the remaining terminals release all the NT in attempt to still send messages

Question 18

Unmasking of Silent Synapses

Answer 18

• (long term potentiation)

- creates new neural pathways by stimulating a synapse to put receptors on the membrane

Question 19

4 Synaptic Changes after CNS injury

Answer 19

• recovery of synaptic effectiveness
• denervation hypersensitivity
• synaptic hypereffectiveness
• unmasking silent synapses

Question 20

Denervation Hypersensitivity

Answer 20

• upregulation of receptors on post synaptic membrane
• Nerves down stream of injury insert more receptors to try to re-establish message
• bad if random NT comes by and inappropriately signals neurons

Question 21

Metabolic Effects of Brain Injury

Answer 21

1. large quantiy of glutamate released from dead/oxygen deprived nerves
2. glutamate binds to NMDA receptors
3. too much calcium into cell–>excitotoxicity

Question 22

Plasticity

Answer 22

• Change in # of connections

- change in strength of connections

Question 23

Experience-Dependent Plasticity

Answer 23

• basis of learning and memory
• turn up strength of synaptic connections (via up regulation)
• aka Long Term Potentiation

Question 24

Mechanism of LTP

Answer 24

• Conversion of silent synapses to active synapses

- change morphology of pre and post synaptic membranes

Question 25

Astrocytes in LTP

Answer 25

• Store and release calcium (for remodeling)
• release glutamate (instigator of remodeling)
• modulate NT release and receptor expression (via Calcium) on post synaptic membrane

Question 26

Initial Response to Peripheral Axon Injury

Answer 26

1. Retraction of Proximal Segment
2. Degeneration Distal Segment
3. Chromatolysis in Cell
4. Effects on Postsynaptic Membrane

Question 27

Too much calcium in the cell–>

Answer 27

1. decreases pH and break down membrane
2. proteases break down cell proteins
3. Oxygen free radicals decrease mitochondria function
4. increase solute concentration in cell and water follow and cause swelling