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Block 5 Week 4 Dani > Von Bartheld Plasticity > Flashcards

Von Bartheld Plasticity Flashcards

1
Q

Explain plasticity?

A

you have a bunch of synapses and end up with much fewer

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2
Q

A mature muscle fiber receives innervation from how many neurons?

A

one

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3
Q

Synapses require a certain minimal level of (blank) support to persist

A

trophic

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4
Q

Where do synapses that want to persist get their nutrition?

A

from factors secreted by postsynaptic (target) cells in response to synaptic activation

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5
Q

Synapses can only utilize trophic support when what two things coincide?

A

their activity and the activiy of the target cell coincide :)

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6
Q

How do nerve fibers get to their desired target and their targets trophic factors?

A

they compete for them, may the best synapse win!

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7
Q

What regulates the competing synapses?

A

the patterning of the pre- and postynaptic activation

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8
Q

What did hubel and wiesel discover about lack of experiences during early postnatal life?

A

showed that the brain translates the effects of early experience (neural activity) into permanantly altered wiring!!!!

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9
Q

where do the afferent fibers of the lateral geniculate nucleus terminate?

A

in the primary visual cortex

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10
Q

The afferent terminals from the lateral geniculate of the eye form an alternating series of eye-specific domains in the cortical layer IV called the (blank)

A

ocular dominance columns

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11
Q

Ocular dominance columns were important in early studies of cortical plasticity, as it was found that monocular deprivation causes the columns in the deprived eye to (blank), with the non-deprived eye assuming control of more of the cortical cells and thus growing. (i.e good eye takes over)

A

degrade

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12
Q

(blank) are stripes of neurons in the visual cortex of certain mammals (including humans) that respond preferentially to input from one eye or the other

A

Ocular dominance columns

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13
Q

The input to from LGN to layer IV is (blank) but cells at the border of the layer IV and above and below layer IV integrate inputs from (Blank) responding to bioncular visual stimuli.

A

segregated

both eyes

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14
Q

If you deprive one eye of vision what will happen to your peripheral visual pathways?

A

nothing, they will remain normal BUT the synapses will not be connected thus you will not be connected to the visual cortex and will be functionally blind in that eye (i.e eye itself fine but the synapses are messed up)

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15
Q

When you get deprivation in one eye during the critical postnatal period, is your cortical blindness (amblyopia) permanent?

A

yes

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16
Q

What happens if an adult gets their eye shut?

A

nothing, they will not become blind and there neurons will remain synapses the way they were previously

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17
Q

Correlated activities between pre and post synaptic terminals equals (blank) bonds

A

stronger bonds

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18
Q

What happens when you have strabismus to your ocular dominance columns and your and binocular neurons in the cortex?

A

ocular dominance columns sharpen

loss of binocular neurons

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19
Q

Cortical neurons in animals with strabismus are driven by (one eye/both eyes)

A

right or left, but not both

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20
Q

Since we know that strabismus can cause loss of binocular neuons and thus binocular vision, what should we do with children who have strabismus?

A

correct there eyes with surgery ASAP before their synaptic connections are made and they lose binocular vision

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21
Q

What is another name for cortical blindness? How can you attempt to fix amblyopia?

A

amblyopia

forcing patient to use weak eye during critical period (i.e alternating eye patches)

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22
Q

What do presynpatic nerve fibers compete for?

A

neurotrophins, trophic factors, NO, NMDA receptors and Ca are involved

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23
Q

What besides ocular dominance occurs during the critical period in cute fluffy animal?

A

imprinting

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24
Q

Imprinting is characterized by a critical period and the relative (blank) of the behavior

A

stability

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25
Q

T/F

social and emotional behaviors require a particular sort of experience during a limited window in early life

A

T

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26
Q

What is super sad about abnormal experiences occuring during the critical period?

A

may induce abnormal patterns of brain circuitry that cannot be rectified later in life :(

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27
Q

Early deprivation of normal experience could lead to (blank).

A

mental disorders (such as neuroses)

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28
Q

A (blank) is an opacity of the lens that prevents normal vision.

A

cataract

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29
Q

Do infants with untreated cataract ever regain normal vision in the eye even after cataract extraction later in life?

A

NOOO

30
Q

Do adults with untreated cataract ever regain normal vision in the eye even after cataract extraction later in life?

A

yes

31
Q

(blank) is the capaicyt of the nervous system to change

A

plasticity

32
Q

Changes in (blank) are prominent during development, but changes in (blank) continues throughout life.

A

wiring

synpases

33
Q

Regulation of the (blank) of synpases is throught to be the mechaism of learning and memory/

A

strength

34
Q

When you have successive action potentials fired close together what will result and why?

A

you will get tetanus from increased Ca and increased neurotransmitter release
(i.e increase synaptic transmission)

35
Q

How can you supress synaptic transmission?

A

rapid succession of action potentials can deplete the neurotransmitter (cuz reuptake is messed up but you still get degredation of neurotransmitter)

36
Q

What happens after the initial period of depression caused by depletion of neurotransmitter and why? What is this called?

A

you get a very large action potential due to the increased amount of calcium that was left over from tetany and huge release of neurotransmitter follows.
Post-tetanic potentiation.

37
Q

Are the changes in synaptic strength long or brief?

A

brief (in the rane of millisecond to minutes)

38
Q

more enduring changes in synaptic strength occur when they serve functions of (blank) and (blank)

A

learning and memory

39
Q

What is long-term potentiation?

A

a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously

40
Q

What is the most prominant and best studied region of the brain relating to LTP?

A

hippocampus

41
Q

Pyramidal neurons in the (blank) region of the hippocampus through schaffer collaterals project to the dendrites of (blank) pyramidal neurons. What is thi pathway involved in?

A

CA3
CA1
human memory (shows robust form of LTP)

42
Q

Electrical stimuliation of schaffer collaterals generates (blank) in postsynaptic CA1 neurons.

A

EPSPs

43
Q

A long-lasting increase in the amplitude of EPSPs can be induced by a brief, high frequency train of stimuli (repetitive activation) to the (blank).

A

Schaffer collaterals

44
Q

LTP can also be induced by (blank) a single stimulus of the schaffer collaterals with a strong depolarization of the postsynaptic neurons. How do you increase the amplitude of the EPSPs? What does this require?

A

pairing
repetitive pairing
coincident activation of pre- and postsynaptic elements

45
Q

In order for both pathways to be strengthened in LTP, you must have both pathways do what?

A

be active together

46
Q

The (blank) of LTP can be explained by the biophysical properties of the NMDA and non-NMDA channels

A

induction

47
Q

During low-frequency stimulation, glutamate is released by the Schaffer by the axons and binds both NMDA and non-NMDA receptors. How come you dont get stimulation of NMDA receptors and only stimulation of non-NMDA receptors?

A

NMDA receptors are blocked by magnesium and the current only flows through the non-NMDA receptors

48
Q

When does the NMDA have current flowing through it and how?

A

during periods of high frequency stimulation or when the postsynaptic site is directly depolarized, the magnesium block is removed from the NMDA receptor

49
Q

What is considered the molecular switch of the LTP?

A

magnesium

50
Q

Besides magnesium, what other ion play an important role in the induction of LTP and what does it do?

A

Calcium, it is a second messenger.

51
Q

(blank)-dependent protein kinases are essential for LTP. What happens when you remove intracellular calcium?

A

calcium

no LTP

52
Q

Insertion of additional (blank) receptors is anther important mechanism to strengthen synapses.

A

AMPA

53
Q

T/F the mechanisms responsible for maintaining LTP are less clear.

A

T

54
Q

How does modification of LTP take place?

A

presynpatically (increase in transmitter release) and postsynaptically (increase in receptor proteins) OR BOTH!

55
Q

To presynpatically modify LTP what do you need?

A

retrograde signals from postysnaptic region to the terminals

56
Q

What are the 2 retrograde factors from the postsynpatic region of LTP?

A

BDNF and NO

57
Q

T/F
experiements with mice carrying a null mutation for BDNF or NO synathase (the enzyme which produces NO) have deficiencies in LTP.

A

T

58
Q

To use LTP what needs to happen to other sets of synapses?

A

they must be weakened

59
Q

What is long term depression (LTD)?

A

weakend set of synapses resulting in a decrease in the size and slope of EPSPS.

60
Q

How do you activate an LTD?

A

NMDA receptors and entry of calcium

61
Q

Low rate stimulation of shaffer collaterals results in (balnk)

A

LTD

62
Q

Small increases in intracellular calcium lead to (LTD/LTP)

A

LTD

63
Q

Large increases in intracellular calcium lead to (LTD/LTP)

A

LTP

64
Q

Small increases of calcium lead to (phosphtase/kinase)

A

phosphatase

kinase for large increases

65
Q

LTP and LTD function through what type of enzymatic modification?

A

phosphorylation. dephosphorylation

66
Q

LTP and LTD regulate the number of (AMPA/NMDA) receptors on the (presynaptic/postsynpatic) membrane.os

A

AMPA

Postsynaptic

67
Q

Issues in LTP leads to what common neurologic disorder?

A

epilepsy

68
Q

What part of the brain is involved in epilepsy?

A

hippocampus

69
Q

(blank) is the repetitive, weak stimulation of the brain that produces long-lasting, irreversible changes in the excitability of the brain.

A

kindling (animal epilepsy)

70
Q

Seizures activate (blank) receptors and strengthen connections between the excited neurons.

A

NMDA

71
Q

(blank) promotes ongoing epileptic activity via strengthened connections between excited neurons.

A

LTP

72
Q

T/F

cortical circuits can be reorganized in adults

A

T

Block 5 Week 4 Dani (14 decks)

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