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Neuroscience > Lecture 13: Neuroplasticity > Flashcards

Lecture 13: Neuroplasticity Flashcards

1
Q

what is neuroplasticity

A

The brain’s ability to modify, change, and adapt throughout life and in response to experience

The connection between neurons can be modified: synaptic plasticity

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2
Q

what are the 3 basic aspects of neuroplasticity

A

Neuroplasticity includes several different processes

It is continually taking place throughout the lifespan

It can be maladaptive in some cases

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3
Q

are connections between neurons static or dynamic

A

dynamic.

there is constant changing based on our experiences

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4
Q

neuroplasticity forms the basis of what?

A

neurorehabilitation

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5
Q

what is Homosynaptic Plasticity

A

Changes in synaptic strength localized to a post-synaptic target neuron stimulated by its own pre-synaptic neuron

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6
Q

what is Heterosynaptic plasticity

A

activity of a neuron leads to changes in the strength of synaptic connections of other neurons

example: Interneurons release other neurotransmitters that act on the synapse

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7
Q

what are the Two main types of Short-Term Plasticity

A

Short-term potentiation

Short-term depression

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8
Q

what is Short-term potentiation

A

Short-term ↑ in synaptic strength

Neurons that fire together, wire together

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9
Q

what is Short-term depression

A

Short-term ↓ in synaptic strength

Neurons that fire out of synch, lose their link

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10
Q

what are the two types of Long-Term Plasticity

A

Long-term potentiation

Long-term depression

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11
Q

what is Long-term potentiation

A

Long-term increase in
synaptic connections

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12
Q

what is Long-term depression

A

Long-term decrease in
synaptic connections

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13
Q

what is the Neuroplasticity Time Frame

A

Short term changes in synaptic strength

  • Temporary functional changes from short term potentiation and depression that take seconds

Long term changes in synaptic strength

  • More permanent, structural changes caused by long term potentiation and depression that take minutes to hours
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14
Q

what are the 4 mechanisms of Long-term potentiation and its result

A

Ca2+ enters the post-synaptic cell to act as a secondary messenger

Glutamate is released from the presynaptic neuron and binds to AMPA receptors

More AMPA receptors are added

↑ in number, size & length of dendritic spines

Results in strengthening of synaptic transmission (LTP)

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15
Q

To change synaptic plasticity on a long-term basis requires which 2 things

A

Gene transcription

Protein synthesis

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16
Q

what are mechanisms for Long-Term Depression

A

Removal of AMPA receptors from post-synaptic membrane

Can’t continually strengthen synapses – needs to be a mechanism to selectively weaken synapses (synapsing pruning)

Low frequency continuous input (the brain doesn’t think something is important)

LTD and LTP have opposing but complementary functions (they abolish each other)

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17
Q

what is the result of Long-Term Depression

A

Postsynaptic membrane is less likely to be depolarized

18
Q

How do our brains know which synapses to strengthen or weaken?

A

Repeated, high frequency stimulation of sufficient amplitude→LTP

Repeated, low frequency stimulation while postsynaptic membrane is hyperpolarized or weakly depolarized→LTD

19
Q

what is the Role of Dopamine in Plasticity

A

Can affect synaptic plasticity by modulating AMPA and NMDA receptors

20
Q

how is CNS injury different from PNS (3 ways)

A

Neuronal death

Overgrowth of glial cells contribute to glial
scarring

Axonal regeneration severely hindered

21
Q

Recovery after brain injury is primarily due to what

A

reorganization of function using remaining intact circuits rather than repair of damaged brain tissue

22
Q

what is an Ischemic stroke

A

Blockage that prevents the brain from getting blood flow

23
Q

what is Penumbra:

A

Reversibly injured brain tissue around ischemic core

24
Q

what is Synaptogenesis

A

Formation of new synapses

main type is reactive synaptogenesis

25
Q

what is Reactive synaptogenesis

A

(collateral sprouting)
* Neighbouring axons sprout to innervate synaptic sites previously activated by injured axons

26
Q

what is Neurogenesis

A

Birth of new neurons

27
Q

what is Cortical Reorganization

A

Sensory and motor maps undergo constant revision so another part of CNS takes over an area of lost function

28
Q

what are the 4 aspects of Experience-Dependent Plasticity

A

Early in learning and after brain injury, many regions of the brain are active

With repetition, the number of active areas decreases because we get more efficient

Cortical reorganization can occur well after injury

These changes are consolidated during sleep

29
Q

what is the relationship with performance and brain activity in Experience-Dependent Plasticity

A

as our performance improves, the amount of brain activity decreased

30
Q

Does Exercise Promote Neuroplasticity?

A

Executive function is most responsive to aerobic exercise

Memory most responsive to resistance training

31
Q

How does Exercise Promote Neuroplasticity? (3 ways)

A

Increases growth factors

Promotes cortical reorganization

Increases the complexity and density of dendritic spines

32
Q

what are the 5 Clinical Implications of neuroplasticity

A

Activities need to be both repetitive and challenging

Need to consider treatment dose when prescribing therapy

Activities must be meaningful

Create an environment that is conducive to plasticity

Activity is important

33
Q

why are Repetitive and Challenging Activities important for neuroplasticity

A

Constraint-Induced Movement Therapy: increased motor map area

Performance of skilled motor tasks promotes neuroplasticity

34
Q

why is Treatment Dose important for neuroplasticity

A

More therapy usually results in better outcomes

Timing also matters

35
Q

why are Meaningful Activities important for neuroplasticity

A

Plays a role in reward, motivation, and reinforcement

dopamine release is linked to the meaningfulness of a task

36
Q

why is Environment important for neuroplasticity

A

Exercise priming (exercise before therapy can decrease GABA (inhibitory) may increase cortical excitability

37
Q

why is Activity is Important for neuroplasticity

A

Prolonged lack of movement can result in loss of function in undamaged adjacent areas

38
Q

Match the correct statement to the type of short-term plasticity

Short-term depression: increase in neurotransmitter

Short-term depression: short-term decrease in synaptic strength

Short-term potentiation: decrease in the availability of neurotransmitter

Short-term potentiation: short-term decrease in synaptic strength

A

Short-term depression: short-term decrease in synaptic strength

39
Q

Which of the following statements are correct regarding homosynaptic and heterosynaptic plasticity?

Interneurons are not involved in homosynaptic plasticity

Homosynaptic plasticity is more localized than heterosynaptic plasticity

All of the responses listed are correct

In homosynaptic plasticity, the postsynaptic neuron is stimulated by its own presynaptic neuron

A

All of the responses listed are correct

40
Q

When Adria’s dog Tui heard the fire alarm go off for the first time which scared her, what likely happened to her synapses within the first few milliseconds or seconds?

Neither structural nor functional changes

Mostly functional changes

Mostly structural changes

Structural and functional changes

A

Mostly functional changes

41
Q

Which of the following responses is true regarding CNS injury in comparison with PNS injury?

There is less neuronal death following CNS injury

There is glial scarring following PNS injury

Axonal regeneration is not possible following CNS injury

Axonal regeneration is very limited following CNS injury

A

Axonal regeneration is very limited following CNS injury

Neuroscience (20 decks)

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