Neuroplasticity 2.0 Flashcards

1
Q

Neuroplasticity

The ability of neurons to change in = ?

three

A

Neuroplasticity (Modifiability): the ability of neurons to change in function, structure, or chemical profile (quantities and types of neurotransmitters produced).

  • Plasticity can occur at synapses, neuronal circuits or neural systems.
  • Plasticity lasts over a long period of time (hours, days and months) and is not periodic.
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2
Q

Define neuroplasticity.

A

Neuroplasticity is the ability of neurons to change in function, structure, or chemical profile.

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3
Q

Neuroplasticity can occur at

  • = ?
  • = ?
  • = ?
A

Neuroplasticity can occur at synapses, neuronal circuits, or neural systems.

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4
Q

How long can plasticity last?

A

Hours, days, and months, and is not periodic.

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5
Q

Neuroplasticity is the basis of all functions involving changes.

  • Examples include = ?
A

Neuroplasticity is the basis of all functions involving changes.

  • Acquisition of new motor skills (e.g., children learning how to ride a bike)
  • Regaining skills lost due to injury to the nervous system (e.g., patients receiving rehabilitation)
  • Acquisition of cognitive skills such as language, music, learning and memory.
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6
Q

How can neuroplasticity affect patients after a nervous system injury?

A

It helps in regaining skills lost due to injury, such as through rehabilitation.

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7
Q

What negative impacts can neuroplasticity have?

A
  • New onset of epilepsy due to cerebral trauma
  • Chronic pain and allodynia following limb amputations are negative impacts of neuroplasticity.
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8
Q

Neuroplasticity encompasses three mechanisms, what are they = ?

A

Neuroplasticity encompasses the following mechanisms:

1) Habituation: Habituation refers to “a decrease in response to a repeated, benign stimulus” (due to a reduced amount of neurotransmitter released from the presynaptic terminal of a sensory neuron)

  • Short-term and can be reversible.
  • One of the simplest forms of neuroplasticity.
  • 5-10 times, 5x/day

2) Experience-dependent plasticity: Complex process involving persistent long lasting changes in the strength of synapse between neurons and neuronal network . Two types of plasticity in excitatory glutamatergic synapses during learning and memory

  • Long term potentiation (LTP)
  • Long term depression (LTD)

3) Cellular recovery after injury: Injuries that damage axons cause. Degeneration but may not result in cell death. Some neurons have ability to regenerate the axon. Injuries that damage cell body = Cell death

  • If the neuron dies, the CNS will work on altering different synapses, change neurotransmitter release and reorganize circuitry.
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9
Q

What is habituation in the context of neuroplasticity?

A

Habituation is a decrease in response to a repeated benign stimulus, a form of neuroplasticity.

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10
Q

How is habituation used in therapies?

A

Habituation techniques and exercises are used to decrease the neural response to a stimulus.

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11
Q

Describe the application of habituation in vestibular disorders.

A

Movements that induce vertigo in vestibular disorders are repeatedly applied to decrease response to dizziness.

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12
Q

What is experience-dependent plasticity?

A

Experience-dependent plasticity involves learning and memory, where persistent changes in synapse strength occur.

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13
Q

What are LTP and LTD?

A

Long Term Potentiation (LTP) and Long Term Depression (LTD) are types of synaptic plasticity in learning and memory.

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14
Q

Describe the cellular mechanism of LTP.

A

LTP involves the conversion of silent synapses to active ones by inserting AMPA receptors into the synaptic membrane.

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15
Q

What happens in LTD at the cellular level?

A

In LTD, AMPA receptors are removed from the synaptic membrane, converting an active synapse to a silent one.

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16
Q

How does environment affect neuroplasticity?

A
  • Animals raised in complex environments have more dendritic branching and synapse production compared to those in non-stimulating environments.
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17
Q

What are the implications of body-weight supported treadmill training?

A

It helps patients regain function and is an example of experience-dependent plasticity in clinical settings.

18
Q

What are stepping pattern generators?

A

- Central / stepping pattern generators (CPG) located within the spinal cord assist with flexion/extension locomotor gait pattern

  • They are neural inputs in the spinal cord that produce rhythmic outputs contributing to stepping and locomotor gait patterns.
19
Q

Explain the role of the cortex in walking post-injury.

A

The cortex assists in postural control and adapts movements to the environment, critical for walking post-injury.

20
Q

What are metabolic effects of brain injury?

A

Following a brain injury like stroke or TBI, neurons can die from lack of oxygen or excitotoxicity caused by excessive glutamate.

21
Q

Describe the concept of synaptic changes following injury.

A

It includes recovery of synaptic effectiveness, denervation hypersensitivity, and other changes in synaptic behavior post-injury.

22
Q

What is the role of Transcranial Magnetic Stimulation in neuroplasticity?

A

TMS can enhance or inhibit motor learning and memory formation, depending on its frequency and protocol.

23
Q

What is task-specific training in stroke rehabilitation?

A

Task-specific training is the systematic, repetitive practice of functional tasks within the available voluntary motion of stroke survivors.

24
Q

How does constraint-induced movement therapy work?

A

It involves engaging the affected upper limbs in intense, task-oriented practice, while the less affected limb is restrained.

25
Q

What principle of neuroplasticity does ‘use it or lose it’ represent?

A

‘Use it or lose it’ means failing to drive specific brain functions can lead to functional degradation.

26
Q

How does ‘use it and improve it’ apply to neuroplasticity?

A

Training a specific brain function can improve its performance, illustrating the ‘use it and improve it’ principle.

27
Q

What does the principle ‘specificity’ suggest in neuroplasticity?

A

Specificity’ suggests that the nature of the training dictates the nature of the plasticity.

28
Q

Why is repetition important in neuroplasticity?

A

Repetition is crucial because it is required for the induction of plasticity.

29
Q

What does the intensity principle in neuroplasticity entail?

A

Sufficient training intensity is necessary for inducing plasticity.

30
Q

Explain the principle that ‘time matters’ in neuroplasticity.

A

Different forms of plasticity occur at different times during the training process.

31
Q

What does the principle ‘salience matters’ mean?

A

Salience matters” emphasizes that training must be functionally relevant to the learner.

32
Q

How does age affect neuroplasticity?

A

Induction of plasticity occurs more easily in younger brains, demonstrating the principle that ‘age matters’.

33
Q

What is the effect of transference in neuroplasticity?

A

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

34
Q

Describe how interference can impact neuroplasticity.

A

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

35
Q

What are long-term changes in neuroplasticity?

A
  • Synthesis of new proteins and growth of new synapses, which maintain memory of specific repetitive stimuli.
36
Q

How can axonal injury in peripheral neurons recover?

A

Damaged axons can regenerate, and new inputs can maintain function at targets deprived of input from injured axons.

37
Q

What adjustments do cortical areas make?

A

Cortical areas adjust to changes in sensory input and develop new functions based on required motor outputs.

38
Q

What can cause cells to die in response to ischemia?

A

Cells can die directly from lack of oxygen or indirectly from events resulting from increased glutamate stimulation.

39
Q

What are the functions of glial scars?

A

Glial scars block axonal regeneration and release growth-inhibiting factors after CNS injuries.

40
Q

Explain the concept of synaptic effectiveness recovery.

A

It occurs when local edema reduces, which previously interfered with neurotransmitter synthesis and action potential conduction.

41
Q

What is denervation hypersensitivity?

A

It occurs when postsynaptic neurons develop new receptors at remaining terminals after presynaptic neurons are destroyed.

42
Q

Describe synaptic hypereffectiveness.

A

It happens when some presynaptic terminals are lost, causing neurotransmitter to accumulate and be excessively released at remaining terminals.