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632: Neuroanatomy-Neuroscience > Neuroplasticity > Flashcards

Neuroplasticity Flashcards

1
Q

What is neuroplasticity?

A

The ability of neurons to change their function, chemical profile, or structure

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2
Q

What are 2 essential characteristics of neuroplasticity?

A
  • It is spatial in that it can occur at all levels

- It is temporal in that it can occur over a long period of time and is not periodic

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3
Q

What is neuroplasticity involved in?

A

Learning and creation of new memories and skills and is essential for recovery from damage to the CNS

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4
Q

Neuroplasticity encompasses what 3 mechanisms?

A
  • Habituation
  • Experience-dependent plasticity (learning and memory)
  • Cellular recovery after injury
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5
Q

What does habituation refer to?

A

a decrease in response to a repeated, benign stimulus

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6
Q

What is habituation due to?

A

a decrease in synaptic activity between sensory neurons and interneurons

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7
Q

PT/OT are techniques and exercises that intended to do what in terms of habituation?

A

decrease the neural response to a stimulus by repeatedly putting a patient in positions of increased sensitivity in hopes to decrease these levels over time

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8
Q

Unlike habituation, learning and memory require what?

A

Experience-Dependent Plasticity

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9
Q

What is experience-dependent plasticity?

A

A complex process involving persistent, long-lasting changes in the strength of synapses between neurons and in neural networks

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10
Q

Describe brain activity during the initial phases of motor learning

A

large and diffuse regions of the brain are active

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11
Q

Describe brain activity when tasks are repeated

A

the number of active regions in the brain are reduced in comparison to the initial phases

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12
Q

Describe brain activity when a task is learned

A

only small, distinct regions of the brain show an increased activity when performing the task

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13
Q

What does experience-dependent plasticity require?

A

The synthesis of new proteins, the growth of new synapses, and the modification of existing synapses

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14
Q

The cellular mechanism for learning and memory results from what 5 things?

A
  • activation of second-messenger systems
  • alteration in the level of intracellular C2+ in the postsynaptic neuron
  • alteration in activity of protein kinase
  • mediate the early stage of synaptic plasticity
  • long-lasting synaptic strength by alteration in the gene transcription
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15
Q

What are the 2 main types of plasticity?

A
  • Long-term potentiation (LTP)

- Long-term depression (LTD)

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16
Q

LTP and LTD can occur presynaptically through what? And postsynaptically through what?

A
  • presynaptically through changes in NT release

- postsynaptically through changes in receptor density and efficiency

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17
Q

Silent vs. Active Synapses

A
  • Silent synapses are characterized by lack of functional glutamate AMPA receptors
  • Active synapses occur when mobile AMPA receptors are inserted into the synaptic membrane
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18
Q

Describe the mechanism of LTP

A

the conversion of silent synapses to active synapses via the activation of NMDA which increases Ca2+ which results in the insertion of AMPA receptors into the cell membrane, which increases the likelihood that the postsynaptic neuron will be depolarized when glutamate is released

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19
Q

Describe the mechanism of LTD

A

the conversion of active synapses to silent synapses by the removal of AMPA receptors from the postsynaptic membrane, making the membrane less likely to be depolarized when glutamate is released from the presynaptic neuron

20
Q

What does Transcranial Magnetic Stimulation (TMS) to the motor complex and other brain areas involved in motor learning do?

A

Enhances or inhibits motor learning and memory formation, depending on the frequency and experimental protocol used

21
Q

Magnetic stimulation of the brain is thought to induce synaptic plasticity via what two things?

A

LTP- or LTD-type mechanisms

22
Q

How do astrocytes contribute to experience-dependent plasticity?

A

Neurons release a NT that stimulates the release of gliotransmitters by the astrocyte which modulate neuronal activity and synaptic transmission

23
Q

How do astrocytes influence synaptic plasticity?

A

Through modulating NT release and receptor expression at the postsynaptic membrane

24
Q

Damage to axons results in what? Damage to the cell body results in what?

A

Injuries that damage or sever axons cause degeneration but may not result in cell death, whereas injury that destroys the cell body of a neuron leads to death of the cell

25
Q

Describe the changes involved in Wallerian degeneration

A

1) the axon terminal degenerates
2) myelin breaks down and forms debris
3) the cell body undergoes metabolic changes
4) presynaptic terminals retract from the dying cell body
5) postsynaptic cells degenerate

26
Q

Following an injury, nervous system goes through a process called what?

A

“sprouting”

27
Q

What are the 2 forms of sprouting?

A
  • collateral

- regenerative

28
Q

Describe collateral sprouting

A

a denervated neuron attracts side sprouts from nearby undamaged axons

29
Q

Describe regenerative sprouting

A

the injured axon issues side sprouts to form new synapses with undamaged neurons

30
Q

Axon recovery typically progresses with a growth rate of __ per day

A

1 mm

31
Q

When should exercise begin following a lesion and why?

A

5 days after lesion to ensure axonal regeneration and muscle re-innervation

32
Q

The functional regeneration of axon occurs due to what?

A

The production of nerve growth factor by Schwann cells

33
Q

Describe the process following axonal injury in the CNS

A

The same processes (retraction, degeneration and chromatolysis) that follows a peripheral axonal injury also occur in the axonal injury in the CNS, however regeneration does not occur

34
Q

Why does regeneration not occur in the CNS?

A

due to glial scars or an absence of nerve growth factor

35
Q

The extent of deficits following damage to the CNS depends on what?

A

the degree of damage to white fiber tracts in the spinal cord and the vertebral level of the injury

36
Q

What are the 4 synaptic mechanisms to overcome damage following CNS injury?

A
  • Recovery of synaptic effectiveness
  • Denervation hypersensitivity
  • Synaptic hypereffectiveness
  • Unmasking of silent synapses
37
Q

How is synaptic effectiveness recovered?

A

When local edema that interferes with action potential conduction is reduced synaptic effectiveness is restored

38
Q

When does denervation hypersensitivity occur?

A

When presynaptic axon terminals are destroyed and new receptor sites develop on the postsynaptic membrane in response to the reduction in the NT released, so when NT are released from nearby axons, there is a hypersensitive response.

39
Q

When does synaptic hypereffectiveness occur?

A

When only some branches of presynaptic axon are destroyed this leads to an accumulation of NT in the undamaged axon terminals, resulting in excessive release of transmitter at the remaining terminals

40
Q

How are silent synapses unmasked?

A

when (AMPA) receptors move into the postsynaptic membrane making the synapse active

41
Q

Cortical representation areas, referred to as cortical maps or homunculus, can be modified by what 4 things?

A
  • sensory input
  • experience
  • learning
  • brain injury
42
Q

Cortical areas routinely adjust to changes in _________ and develop new functions dependent on ___________.

A

sensory input

required motor output

43
Q

Repeated stimulation of somatosensory pathways can cause what? What does this lead to?

A

Increases in inhibitory neurotransmitters which decreases the sensory cortex response to overstimulation

44
Q

Why do oxygen-deprived neurons die?

A

They release large quantities of glutamate which is toxic to neurons

45
Q

What is Excitotoxicity?

A

cell death caused by overexcitation of neurons

46
Q

What are the 3 pathways in which excitotoxicity can occur?

A
  • increased glycolysis
  • increased intracellular water
  • activated protein enzymes
47
Q

What time of training should be done following a stroke and why?

A

task-specific training (as opposed to traditional stroke rehabilitation) because it induces more regular patterns of brain activation

632: Neuroanatomy-Neuroscience (26 decks)

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