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*NEUROMUSCULAR ASPECTS OF EXERCISE > SLE2/MODULE 5- Neuroplasticity > Flashcards

SLE2/MODULE 5- Neuroplasticity Flashcards

1
Q

the nervous system is constantly ____

A

changing
-possibly due to positive things (learning new tasks)
-or not so positive things (disease, aging, injury)

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2
Q

recovery depends on the ability of neurons to do what

A

to reinnervate appropriate targets

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3
Q

2 ways that neurons reinnervate appropriate targets

A

-axon regeneration
-collateral sprouting

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4
Q

axon regeneration

A

regeneration of injured axons

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5
Q

collateral sprouting

A

surviving axons developing sprouts to reinnervate abandoned targets

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6
Q

axotomy

A

axon cut

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7
Q

see slide 6

A
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8
Q

axotomy results in

A

degenerative changes within the axon DISTAL to the legion (distal to where the cut is) + the associated neuron

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9
Q

axotomy- a few days after the cut/lesion occurs, what do we see

A

progression of the black substances (ex: axon + myelin fragments) move about
-Nissl substances break apart + moves to the periphery of the soma; this movement is what will promote the regeneration + ability of sprouting down the axon that is so important to recovery

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10
Q

what does recovery depend on

A

the ability of the axonal sprouts to reinnervate appropriate targets
-so the nature of the injury is vital to success

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11
Q

motor unit

A

refers to the motor neuron projecting from the spinal cord, its axon, + all the muscle fibers that the neuron innervates

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12
Q

3 types of neuron injury

A

-complete transection
-partial denervation
-crush injury

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13
Q

collateral sprouting

A

axons of surviving motor units develop sprouts to reinnervate the muscle fibers that have been denervated

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14
Q

collateral sprouting is confined to what area

A

distal region of motor axon
-occurs close to the target

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15
Q

with collateral sprouting, motor units can enlarge up to ____x the original size

A

5x

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16
Q

see slide 8 graphs

A
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17
Q

what can explain greater force?

a) increased number of fibers innervated
b) large muscle fiber areas
c) greater maximal muscle force per cross-sectional area
d) a + b
e) all of the above

A

e) all of the above

-if I have more fibers innervated, I have a bigger muscle, which means larger muscle fiber area, which means greater amount of force for a given cross-sectional area

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18
Q

neuropathies

A

disorder of PERIPHERAL NERVES

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19
Q

**neuropathies are peripheral or central nerves

A

peripheral

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20
Q

where does the motor axon originate/come out from

A

spinal cord

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21
Q

neuropathies are acute/chronic

A

can be either

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22
Q

neuropathies involve myelin sheath/axon

A

either

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23
Q

what is one of the most common neuropathies

A

diabetic neuropathy
-has to do with blood vessel inability to provide nutrient to the nerve of interest

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24
Q

Guillain-Barre syndrome

A

autoimmune disorder that disrupts myelination of peripheral nerves
-causes neuropathy

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25
Q

what type of neuropathy is caused by Guillain-Barre syndrome

A

rapid-onset acute neuropathy

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26
Q

primary symptoms of Guillain-Barre syndrome

A

-muscle weakness
-tingling (paralysis)

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27
Q

exact cause of Guillain-Barre syndrome

A

unknown
-campylobacter infections (doctors think this disease may be caused by a bacterial infection you can get through food poisoning)

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28
Q

who has Guillain-Barre syndrome

A

Travis Frederick of the Dallas Cowboys

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29
Q

2 autoimmune diseases

A

-GBS (Guillain-Barre syndrome)
-MS (multiple sclerosis)

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30
Q

GBS damages PNS/CNS

A

PNS

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31
Q

MS damages PNS/CNS

A

CNS

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32
Q

autoimmune

A

body’s immune system attacks its own tissues

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33
Q

how does GBS often start

A

post-infection (i.e. respiratory or digestive tract)

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34
Q

how does MS often start

A

likely due to:
-infections (i.e. Epstein-Barr virus or herpes)
-genes
-vitamin D deficiency
-smoking

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35
Q

GBS common symptoms

A

-weakness
-numbness
-tingling in limbs

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36
Q

MS common symptoms

A

-weakness
-numbness
-tingling in limbs

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37
Q

GBS prognosis

A

-severe symptoms
-full recovery possible

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38
Q

MS prognosis

A

lifelong disease
-varying symptom duration

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39
Q

can someone have GBS + MS at same time

A

very rare but not impossible
-coincidence if it does occur

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40
Q

similarities between GBS + MS

A

both are:
-de-myelinating conditions
-influence the nervous system
-autoimmune

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41
Q

neurogenesis

A

ability to generate neurons

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42
Q

neurogenesis may have what concerns

A

ethical

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43
Q

neuroplasticity in response to disease

A

-possibility to transform skin cells into induced pluripotent stem cells + then differentiate into neurons
-cultured human neurons with potential therapeutic application to neurological disorders + injuries (Alzeimer’s, Parkinson’s, Huntington’s, Epilpsy, Stroke)

-neurogenesis may have ethical concerns + therefore isn’t a common response to some of these diseases

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44
Q

neuroplasticity in response to injury

A

-largely involves synaptogenesis

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45
Q

neuroplasticity occurs at what 2 levels

A

-individual
-population

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46
Q

**population level of neuroplasticity

A

changes in:
-thickness
-volume
-density

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47
Q

functional changes of neuroplasticity have to do with

A

activities that pertain to electrical signals being transmitted or some sort of neurotransmitter crossing a synaptic cleft

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48
Q

neuroplasticity functional changes (3)

A

-EPSP/IPSP
-synaptic activity
-intrinsic excitability

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49
Q

EPSP/IPSP

A

the electrical response to a depolarizing/hyperpolarizing singal

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50
Q

synaptic activity

A

the release of vesicles neurotransmitters

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51
Q

intrinsic excitability

A

excitability inherent to the neuron

52
Q

structural changes of neuroplasticity have to do with

A

the actual properties you can look at under a microscope

53
Q

neuroplasticity- structural changes (4)

A

-dendritic arbors
-spine density
-synapse number + size
-receptor density

54
Q

dendritic arbors

A

growth of little dendrites + sprouts

55
Q

spine density

A

size of spines + sprouts

56
Q

synapse number + size

A

you can evaluate + measure with tiny rulers in your microscope

57
Q

receptor density

A

number of receptors you have
(if I take a certain drug will I have more synapses/more receptors? if i have this injury occur, will there be changes to the structure of my system?)

58
Q

where do changes from neuroplasticity take place (2)

A

-synapse (synaptic)
-cell (structural)

59
Q

neuroplasticity changes at synapse

A

-changed amount of neurotransmitter released for each AP discharged at axon terminal
-at postsynaptic membrane, changed number of receptors for neurotransmitter, type of neurotransmitter receptors, or second messenger release

60
Q

neuroplasticity changes at cell (structural) level

A

change in number of synapses (dendrites, branches, length) or even numbers of neurons (sprouting, pruning)

61
Q

neuroplasticity changes at synapse are short/long term

A

can be either

62
Q

neuroplasticity changes at cell (structural) are short/long term

A

long term

63
Q

which of these is the best example of structural neuroplasticity at the population level?

a) increased acetylcholine release at a neuromuscular junction
b) calcium release due to a G-protein couple receptor effect within a neuron
c) greater presynaptic inhibition by one neuron projecting onto another
d) increased grey matter volume
e) one neuron’s synapses become larger

A

d) increased grey matter volume

64
Q

estimating structural adaptations

it is possible to measure thickness of selected brain regions as an index of ____

A

dendritic content change

65
Q

estimating structural adaptations

how are functional changes measured

A

-extracellular recordings of field potentials (EEG, evoked potentials)
-imaging (fMRI, PET)

66
Q

estimating structural adaptations

measuring what of the cerebral cortex reveals changes

A

size of sensory + motor maps of cerebral cortex

67
Q

motor map

A

looks at changes in cortex related to motor functions

(if you acquire a motor skill like cup stacking, you should be able to see changes in the motor map associated with the action but in your brain)

68
Q

sensory map

A

generating by looking at brain activity/responses to incoming stimuli

(whereas motor maps are made by directly stimulating the brain itself)

69
Q

motor maps in the cortex can be measured with ____

A

intracortical microstimulation

70
Q

3 ways motor maps in the cortex are measured with intracortical microstimulation

A

-areas of the cortex in which stimulation evokes movement
-placement of the stimulating electrode
-trans-synaptic activation of corticospinal neurons

71
Q

3 ways cortex motor maps are measured w/ intracortical microstimulation

areas of cortex in which stimulation evokes movement

A

motor map of the cortex, shows areas of the cortex where stimulation happened that evoked movement

-we see the movements are associated with the whisker of a rodent in pink, we see there is a change that occurred distally in green, etc.

72
Q

3 ways cortex motor maps are measured w/ intracortical microstimulation

placement of the stimulating electrode

A

we see placement of the stimulating electrode via the needle like thing in the transection related to the nervous system

73
Q

3 ways cortex motor maps are measured w/ intracortical microstimulation

trans-synaptic activation of corticospinal neurons

A

we see trans-synaptic (trans = across) activation of corticospinal neurons; looking at motor maps + changes you can see in

-response to the stimulus at the CNS in the spinal cord + how that affects a bunch of different neurons

74
Q

several weeks of skilled reach training increased what 2 things in rat motor cortex

A

-size of distal motor map
-increased synaptic density

75
Q

much more increase for skilled or unskilled reaching for rodent motor cortex

A

SKILLED

76
Q

explain how rat housing conditions influenced neuron structure

A

much more extensive branching in enriched castle
-raised cortical neurons
-more extensive dendrites + dendritic spines

77
Q

motor recovery depends on changes in ____

A

synaptic function

78
Q

what 2 ways is motor recovery/rehabilitation accomplished

A

-recovery
-compensation

79
Q

recovery

A

-restoration of function in neural tissue that was initially lost due to injury/disease
-usually explained by gradual removal of responses to injury (edema inflammation, blood flow disturbance)

ex: I experience an injury at the gym + with time I am able to recover fully/close to fully

80
Q

what is the most common way that acute injuries are responded to

A

recovery

81
Q

compensation

A

-residual neural tissue takes over a function that has been lost due to injury/disease
-possibly due to redundancy that exists in the cortex

ex: I can get a sensory/motor map in multiple areas of certain regions of the brain + can see that there are regions of the brain dedicated to the same task/sensory response
-SO if one area is damaged, I can use another area to compensate for the damaged area to make sure I don’t lose the ability to do an action

82
Q

compensation is due to ____

A

redundancy

83
Q

example of RECOVERY after loss of function in residual neural tissue after an injury

A

-after the stroke, the rodent is not able to move the forelimb/activate the associated regions of the brain to do the forelimb movement as well as it did before the stroke
-not all is lost because there are SOME regenerations/recovery only 24 hours after + with time there will be more

*motor map via intracortical microstimulation (ICMS) of forelimb movements (green) in rat motor cortex before (left) and 24 hrs after (right) focal stroke (dotted line)

*loss of movements outside stroke area was accompanied by a loss of synapses (graph) at 24 hrs after the stroke

84
Q

example of COMPENSATION after injury

A

-a stroke as induced, + rather than recovering the same areas as before, the brain compensated for the now damaged locations

*motor maps for hand movements in the ventral premotor cortex (PMV) of a monkey before and after a stroke
*hand representation in the PMV increased in size after the stroke
*the PMV became more involved in hand movements than it was before the stroke

85
Q

when is functional improvement the greatest

A

when it involves recovery

-nothing is as great as fixing what has already been damaged (ex: teacher is out sick, no one can replace the teacher the same way as if the teacher came back)

86
Q

when is functional improvement the least

A

when it is based on compensation

87
Q

strategies to improve motor function (3)

A

-restoration
-recruitment
-retraining

88
Q

strategies to improve motor function- restoration

A

refers to activating brain areas in which function has been compromised
-progressive but doesn’t begin until after injury

89
Q

**strategies to improve motor function- restoration involves recovery/compensation

A

recovery

90
Q

strategies to improve motor function- recruitment

A

-enlists brain areas with the ability to produce motor function but are not involved in action pre-injury
-occurs when damage to neural tissue cannot be resolved
-is not due to secondary effects of injury

91
Q

**strategies to improve motor function- recruitment involves recovery/compensation

A

compensation
-but does not involve learning new functions

92
Q

strategies to improve motor function- retraining

A

form of compensation in which residual neural tissue is required to learn a new function

93
Q

**strategies to improve motor function- retraining involves recovery/compensation

A

compensation

94
Q

pre-stroke + post-stroke groups with no motor rehabilitation vs motor rehabilitation

A

several days of training on the forelimb reaching task restored both movement representations and synaptic density

95
Q

pre-stroke + post-stroke groups with no motor rehab vs motor rehab

compare both pre-stroke panels

A

not a big difference between motor rehab vs no motor rehab

96
Q

pre-stroke + post-stroke groups with no motor rehab vs motor rehab

compare post-stroke panels

A

motor rehab is much more successful than no motor rehab

97
Q

which statement about neural plasticity is incorrect?

a) enriched housing increases the size of motor maps
b) it is unlikely that the region of an evoked stroke will be recovered with rehabilitation
c) sensory maps are measured by stimulating peripheral receptors + measuring the cortical response
d) unskilled reaching increases the motor maps for distal muscles
e) specific movement training like reaching tasks by rodents can influence motor maps

A

d) unskilled reaching increases the motor maps for distal muscles

98
Q

LTP

A

long term potentiation

99
Q

LTP increases what

A

size/amplitude of EPSPs
-and generates new dendritic spines

100
Q

LTD

A

long term depression

101
Q

what is the key factor underlying changes in motor + sensory maps

A

changes in synaptic function

102
Q

what is the most characterized change in synaptic function

A

LTP + LTD

103
Q

what 3 things does LTP depend on

A

-intensity
-repetition
-timing of the activating signal

104
Q

intensity

A

how QUICKLY we stimulate
-aka rate of stimulation

105
Q

change in EPSP amplitude in rat hippocampus slice depends on what

A

rate of stimulation (aka intensity)

106
Q

tetanic stimulation at a lower/higher frequency augments EPSP more

A

higher frequency
-lower frequency does go up but not very much
-so in response to that the system drops + the EPSP becomes smaller
-after the stimulation stops that deduction below the baseline value is LTD

107
Q

higher LTP…

A

the longer it will stay

108
Q

LTP in the rat cortex was greater after receiving the stimulation for 1 day or 5 days

A

5 days
-this indicates the influence of REPETITION

109
Q

coactivation

A

2 neurals input at same time, concurrent input
-output is strengthened

110
Q

what 4 things does synaptic strength depend on

A

-quantity of neurotransmitter
-number of postsynaptic receptors
-synapse size
-number of synapses

111
Q

salience

A

the quality of being particularly noticeable/important
-aka the prominence/significance of the test we are doing + the intervention induced to it

112
Q

occipital

A

related to vision

113
Q

frontal cortex

A

related to being able to name different objects

114
Q

besides intensity, repetition, + timing what 2 things does neural plasticity depend on

A

specificity + salience of the intervention

115
Q

rats trained on 4 tasks produced specific adaptations- visuospatial learning (Morris water maze)

A

increased dendritic length + branching on pyramidal cells in occipital cortex

116
Q

rats trained on 4 tasks produced specific adaptations- object recognition

A

increased dendritic branching + spine density in frontal cortex

117
Q

rats trained on 4 tasks produced specific adaptations- skilled reaching

A

increased dendritic legnth + branching in contralateral forelimb cortex

118
Q

rats trained on 4 tasks produced specific adaptations- bilateral string pull

A

same changes in both sides of cortex

119
Q

experiment- rats trained to discriminate between frequency + loudness

A

test of salience

-all of the rodents received recordings related to frequency + loudness; but the rodents were specifically trained on only ONE of them
-control group- had no training on either frequency or loudness discrimination
-frequency discrimination group- only trained on frequency / vice versa for loudness discrimination group
-map is way bigger in frequency discrimination group than the loudness discrimination group for the frequency map

120
Q

which factor does not influence the size of LTP?

a) intensity
b) timing
c) repetition
d) number of dendritic spines
e) salience

A

d) number of dendritic spines

because number of dendritic spines is typically part of the output

121
Q

neural plasticity provides a foundation for ____

A

neurorehabilitation

122
Q

training can increase the size of what 3 things

A

-motor maps
-sensory maps
-visual maps

123
Q

how do map changes reflect adaptations

A

in the number, density, + function of synapses

124
Q

what 4 things does synaptic plasticity (e.g. LTP) depend on

A

-intensity
-repetition
-timing
-salience

(of the activating signal)

125
Q

functional improvements are possible, with a preference for recovery/compensation

A

recovery

*NEUROMUSCULAR ASPECTS OF EXERCISE (9 decks)

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