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632: Neuroanatomy-Neuroscience > Neuroplasticity > Flashcards

Flashcards in Neuroplasticity Deck (47):
1

What is neuroplasticity?

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

2

What are 2 essential characteristics of neuroplasticity?

- 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

3

What is neuroplasticity involved in?

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

4

Neuroplasticity encompasses what 3 mechanisms?

- Habituation
- Experience-dependent plasticity (learning and memory)
- Cellular recovery after injury

5

What does habituation refer to?

a decrease in response to a repeated, benign stimulus

6

What is habituation due to?

a decrease in synaptic activity between sensory neurons and interneurons

7

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

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

8

Unlike habituation, learning and memory require what?

Experience-Dependent Plasticity

9

What is experience-dependent plasticity?

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

10

Describe brain activity during the initial phases of motor learning

large and diffuse regions of the brain are active

11

Describe brain activity when tasks are repeated

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

12

Describe brain activity when a task is learned

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

13

What does experience-dependent plasticity require?

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

14

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

- 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

15

What are the 2 main types of plasticity?

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

16

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

- presynaptically through changes in NT release
- postsynaptically through changes in receptor density and efficiency

17

Silent vs. Active Synapses

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

18

Describe the mechanism of LTP

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

19

Describe the mechanism of LTD

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

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

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

21

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

LTP- or LTD-type mechanisms

22

How do astrocytes contribute to experience-dependent plasticity?

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

23

How do astrocytes influence synaptic plasticity?

Through modulating NT release and receptor expression at the postsynaptic membrane

24

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

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

Describe the changes involved in Wallerian degeneration

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

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

“sprouting”

27

What are the 2 forms of sprouting?

- collateral
- regenerative

28

Describe collateral sprouting

a denervated neuron attracts side sprouts from nearby undamaged axons

29

Describe regenerative sprouting

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

30

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

1 mm

31

When should exercise begin following a lesion and why?

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

32

The functional regeneration of axon occurs due to what?

The production of nerve growth factor by Schwann cells

33

Describe the process following axonal injury in the CNS

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

Why does regeneration not occur in the CNS?

due to glial scars or an absence of nerve growth factor

35

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

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

36

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

- Recovery of synaptic effectiveness
- Denervation hypersensitivity
- Synaptic hypereffectiveness
- Unmasking of silent synapses

37

How is synaptic effectiveness recovered?

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

38

When does denervation hypersensitivity occur?

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

When does synaptic hypereffectiveness occur?

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

How are silent synapses unmasked?

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

41

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

- sensory input
- experience
- learning
- brain injury

42

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

sensory input

required motor output

43

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

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

44

Why do oxygen-deprived neurons die?

They release large quantities of glutamate which is toxic to neurons

45

What is Excitotoxicity?

cell death caused by overexcitation of neurons

46

What are the 3 pathways in which excitotoxicity can occur?

- increased glycolysis
- increased intracellular water
- activated protein enzymes

47

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

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