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Neuroscience > Lecture 14 Neuroplasticity > Flashcards

Lecture 14 Neuroplasticity Flashcards

1
Q

What is neuropraxia?

A
  • local myelin damage
  • axon remains intact
  • results in slow AP (mild weakness, tingling)
  • symptoms are mild or transient (short time)
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2
Q

What is axonotemesis?

A
  • continuity of axon is lost

- loss of continuity leads to Wallerian degeneration (degeneration distal to injury)

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3
Q

What is neurotmesis?

A

complete transection of nerve

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4
Q

What axonal injury is the least severe?

A

neuropraxia

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5
Q

What axonal injury is the most severe?

A

neurotmesis

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6
Q

Describe the steps that occur after a peripheral nerve is injured that has the potential to regrow

A

1) Wallerian degeneration (degeneration distal to injury)
2) macrophages clear debris AND Schwann cells become phagocytic to degenerating axon and myelin
3) central end of axon tunnels into endoneurial sheaths left behind
4) Schwann cells increase as axon regrows - help produce new myelin and guide axon regrowth
5) axon re-establishes postsynaptic target
6) axon diameter increases, more myelin created

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7
Q

What is Wallerian degeneration?

A

degeneration of axon distal to injury

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8
Q

What are the two different types of axonal sprouting?

A
  • collateral

- regenerative

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9
Q

What is collateral axonal sprouting?

A

start with 2 neurons, 1 dies and doesn’t regrow, but neighboring neurons help hit postsynaptic receptors

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10
Q

What is regenerative axonal sprouting?

A

start with 2 neurons, 1 degenerates, then regrows back to postsynaptic receptor

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11
Q

Why can’t the CNS regenerate?

A
  • CNS damage triggers necrosis and apoptotic (release neurotoxins) cell death down whole neuron
  • clean up is slow due to lack of schwann cells (oligodendrocytes in CNS) and macrophages
  • astrocytes causes glial scarring
  • microglial activation - can’t tell what is good and bad
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12
Q

What HAS been shown to have neurogenesis capabilities? Where in the CNS can these structures be found?

A
  • glial cells (support cells)

- found in Olfactory bulb and Hippocampus

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13
Q

Define neuroplasticity. In general, how does it work?

A
  • Ability of CNS to change its chemical profiles, structure, and function in response to a given stimuli or situation
  • Activated by environmental, behavioral, or neural processes
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14
Q

What is chemical neuroplasticity?

A
  • see when we start to use a pathway repetitively
  • immediate to short-term changes to chemical synapses
  • increase neurotransmitters released into synaptic cleft
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15
Q

What is structural neuroplasticity?

A
  • long-term changes to neuronal structure
  • modify existing postsynaptic receptors
  • create new postsynaptic receptors
  • increase dendritic growth
  • increased terminal axons
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16
Q

What is functional neuroplasticity?

A
  • long-term changes to the neuronal function

- Neurons change roles, function, and information being relayed

17
Q

What is cortical remapping? What are some examples?

A
  • Process in which the existing cortical “map” is affected, and ultimately changed, by a stimulus
  • blindness (other senses are stronger)
  • phantom limb
18
Q

What is habituation?

A
  • simplest form of neuroplasticity
  • When our brain decides to decrease its sensitivity or response to repeated and benign stimulus
  • lets us pay attention to what is important and what is not

ex: young vs old snoring couple

19
Q

What is short-term habituation?

A

< 30 minutes

  • changes pre-synaptic (decrease release of excitatory neurotransmitters)
  • effects are transient (short term and no structural changes)
20
Q

What is long-term habituation?

A

> 30 minutes

- changes post-synaptic (decrease receptors on postsynaptic)

21
Q

What drives our ability to learn and remember? Through what processes is this manifested?

A

past experience

Long-term potentiation and depression

22
Q

What is long-term potentiation? What is required to see this process occur?

A
  • major way for the brain to increase sensitivity
  • synaptic connections between neurons become stronger by frequent activation
  • Requires high intensity stimulation
23
Q

What receptors are involved in long-term potentiation?

A

AMPA

NMDA

24
Q

What are AMPA receptors permeable to and how do they respond?

A
  • permeable to Na+

- glutamate binds to ligand receptor causing them to open and let Na+ through

25
Q

What are NMDA receptors permeable to and how do they respond?

A
  • permeable to Na+ and Ca2+

- contain Mg2+ blockade that must be moved by lots of Na+ before Ca2+ and more Na+ can flow in

26
Q

What is occurring when we see electrostatic repulsion during long-term potentiation?

A
  • higher/faster AP which leads to more neurotransmitter (glutamate) into synaptic cleft
  • more glutamate binds to AMPA receptors causing increase in Na+ in postsynaptic cell
  • electrostatic repulsion occurs by increase in postsynaptic Na+ pushing Mg2+ blockade from NDMA receptor
  • Ca2+ and Na+ flow in through NDMA receptor for long-term potentiation
27
Q

Why are NMDA receptors referred to as “coincidence receptors?”

A

Requires specific pre- and postsynaptic events to open

28
Q

Why is calcium important in long-term potentiation?

A
  • Secondary messenger that activates secondary intracellular cascades in postsynaptic cell for STRUCTURAL CHANGES
  • increase postsynaptic AMPA receptors
  • increase growth factors which leads to new synapses
29
Q

In general, what is thought to occur during long-term depression? Why do we need this process to occur?

A
  • reset button
  • Conversion of active synapses into silent ones
  • helps clear the slate for synapses to perform a new task
30
Q

Explain use it or lose it

A

Failure to drive specific brain functions can lead to functional degradation

31
Q

Explain use it and improve it

A

Training that drives a specific brain function can lead to an enhancement of that function

32
Q

Explain specificity matters

A

The nature of the training experience dictates the nature of the plasticity

33
Q

Explain repetition matters

A

Induction of plasticity requires sufficient repetition

34
Q

Explain intensity matters

A

Induction of plasticity requires sufficient training intensity

35
Q

Explain time matters

A

Different forms of plasticity occur at different times during training

36
Q

Explain salience matters

A

The training experience must be sufficiently salient (most noticeable) to induce plasticity

37
Q

Explain age matters

A

Training-induced plasticity occurs more readily in younger brains

38
Q

Explain transference or generalization

A

Plasticity in response to one training experience can enhance the acquisition of similar behaviors

39
Q

Explain interference

A

Plasticity in response to one experience can interfere with the acquisition of other behaviors

Neuroscience (16 decks)

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