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Development/ Plasticity > Exam 3 Practice Questions > Flashcards

Exam 3 Practice Questions Flashcards

1
Q

In the central nervous system, which cells myelinate axons?
a. Microglia
b. Schwanncells
c. Oligodendrocytes
d. Astrocytes

A

C. Oligodendrocytes

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2
Q

In the peripheral nervous system, which cells myelinate axons?
a. Microglia
b. Schwann cells
c. Oligodendrocytes
d. Astrocytes

A

B. Schwann cells

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3
Q

Central nervous system axons
a. Regenerate better than peripheral axons
b. Regenerate more poorly than peripheral axons
c. Regenerate quicker than peripheral axons
d. Regenerate in the opposite direction of the lesion

A

b. Regenerate more poorly than peripheral axons

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4
Q

What is a likely source of signals preventing central axon regeneration?
a. Schwann cells
b. Oligodendrocytes
c. Osteoblasts
d.Stem cells

A

b. Oligodendrocytes

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5
Q

Comparisons of what types of cells led to the discovery of several types of signals preventing regeneration
a. Osteoblasts and osteoclasts
b. Astrocytes and osteoblasts
c. Oligodendrocytes and Schwann cells
d.Schwann cells and stem cells

A

c. Oligodendrocytes and Schwann cells

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6
Q

Which hippocampal pathway exhibits a presynaptic mechanism of LTP?
a. Schaffer collateral
b. Commissural pathway
c. Mossy fiber pathway
d. Direct perforant pathway

A

c. Mossy fiber pathway

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7
Q

Mossy fiber LTP requires activation of which
a. NMDA receptors
b. L-type calcium channels
c.PKA
d.CamKII

A

C. PKA

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8
Q

Mossy fiber LTP can be induced by
a.Carefully timing presynaptic spikes with postsynaptic spikes
b.Tetanic presynaptic stimulation
c.It can’t be induced
d. All of the above

A

b. Tetanic presynaptic stimulation

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9
Q

Which of the following enzymes is activated in the post-synaptic cell when the facilitating interneuron activates it? (regraded; idk the answer)
a. PKG
b. FYN
c. PKA
d. Calmodulin

A

c. PKA

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10
Q

LTP in the Schaffer collateral and the direct perforant pathway differs in the presence of which of the following mechanisms?
a. NMDA receptors
b. Shaker potassium channels
c. L-type calcium channels
d. Calmodulin

A

c. L-type calcium channels

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11
Q

Which of the following hippocampal pathways are associative
a. Commissural pathway
b. Direct perforant pathway
c. Schaffer collateral
d. All of these

A

c. Schaffer collateral

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12
Q

In the presynaptic mechanism of hippocampal LTP, which is the coincidence detector?
a. NMDA receptors
b. There is no coincidence detector
c. Adenylyl cyclase
d. Calmodulin

A

b. There is no coincidence detector

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13
Q

In a synapse that can engage in postsynaptic LTP, what is the most likely cause of LTD instead of LTP?
a. NMDA activation
b. AMPA activation
c. Long slow calcium current
d. Rapid calcium current

A

c.Long slow calcium current

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14
Q

What is the main difference between early vs late phase LTP
a. CaMKII activation
b. Gene expression
c. Calcineurin activation
d. Calmodulin activation

A

b. gene expression

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15
Q

Which of the following mechanisms is involved in increasing the sensitivity of a synapse expressing the postsynaptic mechanism of LTP
a. NMDA dephosphorylation
b. L-type calcium channel phosphorylation
c. AMPA phosphorylation
d. Potassium channel phosphorylation

A

b. L-type calcium channel phosphorylation

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16
Q

In a synapse that can engage in postsynaptic LTP, what is the most likely cause of LTD instead of LTP?
a. Calmodulin activation
b. Rapid large calcium current
c. Calcineurin activation
d. AMPA activation

A

c. Calcineurin activation

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17
Q

Which hippocampal pathway has a presynaptic mechanism of LTP?
a. Commissural
b. Schaffer collateral
c. Mossy fibers
d. Direct perforant

A

C. Mossy fibers

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18
Q

In the presynaptic mechanism of hippocampal LTP, how do we know it is presynaptic?
a. Blocking calcium channels blocks the effect
b. Blocking PKA has no effect
c. Blocking PKA blocks the effect
d. Blocking NMDA receptors blocks

A

a. Blocking calcium channels blocks the effect

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19
Q

Which of the following mechanisms is involved in increasing the sensitivity of a synapse expressing the postsynaptic mechanism of LTP?
a. Phosphorylation of L-type calcium channels
b. Calcineurin activation
c. Insertion of new AMPA receptors
d. Insertion of new NMDA receptors

A

c. Insertion of new AMPA receptors

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20
Q

Spike timing-dependent plasticity, where cell A is presynaptic cell B, which of the following scenarios would result in strong LTD?
a. Cell B intermittently fires long before cell A
b. Cell B consistently fires immediately before cell A
c. Cell A consistently fires immediately before cell B
d. Cell A intermittently fires long before cell

A

a. Cell B intermittently fires long before cell A

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21
Q

Regarding spike-timing-dependent plasticity, where cell A is presynaptic to cell B, which of the following scenarios would result in strong LTP?
a. Cell A consistently fires immediately before cell B
b. Cell B consistently fires immediately before cell A
c. Cell B intermittently fires long before cell A
d. Cell A intermittently fires long before cell B

A

a. Cell A consistently fires immediately before cell B

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22
Q
  1. During hippocampal LTP, increased EPSPs can result from:
    a. Insertion of vesicles carrying AMPA receptors into the plasma membrane
    b. Dephosphorylation of membrane AMPARS
    c. Phosphorylation of membrane AMPARS
    d. Activation of protein phosphatases
    e. A and C
    f. C and D
A

e. A and C

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23
Q

The late phase of LTP requires the activation of additional molecular processes in the postsynaptic neuron compared to the early phase. One example of that additional mechanism is:
a. Activation of protein phosphatases
b. Activation of protein kinases
c. Insertion of additional AMPARS into the postsynaptic membrane
d. Protein synthesis de novo (synthesis of new proteins) and gene expression
e. Internalization of membrane NMDARS (pulling NMDARS from the membrane into the cytosol)

A

d. Protein synthesis de novo (synthesis of new proteins) and gene expression

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24
Q

NMDARS and AMPARS are
a. Ligand-gated receptors
b. Neurotransmitter-gated ion channels
c. Ionotropic receptors
d. Cation-permeable channels
e. All of the above
f. None of the above

A

e. all of the above

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25
Q

Both AMPA and NMDA receptor types require postsynaptic membrane depolarization as well as ligand binding to open
a. True
b. False

A

a. True

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26
Q

What do you know about AMPA receptor phosphorylation in the postsynapse during LTP?
a. It leads to an increase in subsequent EPSPS
b. It is mediated by protein phosphatases
c. It leads to less active AMPARS
d. It requires very small calcium increases

A

a. It leads to an increase in subsequent EPSPS

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27
Q

The induction of LTP at a given synapse is independent of the activity of the presynaptic cell
a. True
b. False

A

b. False

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28
Q

LTP and LTD are types of plasticity neuronal networks used to encode relevant (important) vs nonrelevant information
a. True
b. False

A

a. True

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29
Q

The reason why NMDARS do not open simply because their ligand is bound to them is because the receptor channel’s pore is occupied by a manganese ion, which needs to be expelled by membrane depolarization
a. True
b. False

A

a. True

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30
Q

Behavioral sensitization, mediated by synaptic facilitation of the gill withdrawal reflex in Aplysia is mediation by connections between the ________ interneuron from the tail and the sensory neurons innervating the terminal of the ________ and the mantle.

A

Behavioral sensitization, mediated by synaptic facilitation of the gill withdrawal reflex in Aplysia is mediation by connections between the facilitated interneuron from the tail and the sensory neurons innervating the terminal of the siphon and the mantle.

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31
Q

This interneuron from the tail releases ________ on the pre-synaptic terminal of the ____ and the siphon mantle.

A

This interneuron from the tail releases 5HT on the pre-synaptic terminal of the Siphon and the siphon mantle.

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32
Q

This neurotransmitter then activates two separate receptors, the first Gq/11 protein-coupled receptor activates ________, which is a membrane-bound protein that diffuses through the membrane and cleaves ____ into inositol triphosphate and DAG

A

This neurotransmitter then activates two separate receptors, the first Gq/11 protein-coupled receptor activates PKC, which is a membrane-bound protein that diffuses through the membrane and cleaves PIP2 into inositol triphosphate and DAG

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33
Q

____________ then translocate to the membrane where it first interacts with phosphatidyl serine and then _________ which removes the pseudosubstrate from the catalytic cavity

A

PKA then translocate to the membrane where it first interacts with phosphatidyl serine and then ligands which removes the pseudosubstrate from the catalytic cavity

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34
Q

This enzyme then diffuses through the membrane and interacts with its catalytic targets namely voltage-gated ________ channels and the neurotransmitter release and vesicle recruitment machinery

A

This enzyme then diffuses through the membrane and interacts with its catalytic targets namely voltage-gated Ca2+ channels and the neurotransmitter release and vesicle recruitment machinery

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35
Q

The other g protein-coupled receptor, the ____protein-coupled receptor activates ____ which converts ATP to ____ binds the inhibitory subunits, and releases the catalytic subunits of the enzyme_____

A

The other g protein-coupled receptor, the Gs protein-coupled receptor activates **adenyl cyclase ** which converts ATP to cAMP binds the inhibitory subunits, and releases the catalytic subunits of the enzyme PKA

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36
Q

This kinase phosphorylates voltage-gated __________ ion channels, voltage-gated ________ ion channels, and the neurotransmitter release and vesicle recruitment machinery, enhancing the release of NT into the synapse

A

This kinase phosphorylates voltage-gated Ca2+ ion channels, voltage-gated K+ ion channels, and the neurotransmitter release and vesicle recruitment machinery, enhancing the release of NT into the synapse

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37
Q

What type of pre-synaptic stimulation will cause LTD instead of LTP?

A

Post before pre

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38
Q

What differs in the mechanism to induce LTD instead of LTP (think Calcium and how it activates what)?

A

Small increases in Ca2+

39
Q

What type of presynaptic stimulation will cause LTD instead of LTP?

A

Low-frequency stimulation ( or pre-synaptic firing) leads to depression in the post-synaptic cell. EPSP is going to be lower than the baseline EPSP

40
Q

Characterize STDP with Hebbian or Anti-Hebbian with bias

A
  • Even curve in quadrance 2 and quadrant 3 –> hebbian (classic, not biased)
  • Curve with a bump on top in quadrant 2, smaller curve in quadrant 3 –> Hebbian (LTP-biased)
  • Only valley below the x-axis in quadrants 3 and 4 –> anti-hebbian (LTD only)
41
Q

For each question answer with large or small LTP or LTD

a. Regarding Figure A what type of LTP will result with a large positive delta t?
b. Regarding Figure B what type of plasticity will result from a small negative delta t?
c. Regarding Figure C what type of plasticity will result from a small positive LTP?

disregard red numbers

A

a. small LTP because of no changein plasticity and there is no indication of coincidence so nothing will change
b. small LTD
c. large LTD

42
Q

In a sentence describe how NMDA receptors are activated and what type of current results

A

In LTP NMSA activation comes from depolarization in glutamate and a large influx of calcium renders LTP current

43
Q

Describe the difference between sensitization and classical conditioning. Your answer should be very specific and include ( but not be limited to) differences in the experimental paradigm, behavioral response, as well as cellular and molecular differences in the process. The sensitization paradigm includes one poking the siphon, shocking the tail, and then poking the siphon again. The result of this paradigm is that the gill then withdraws for all types of stimulus, including harmless stimuli in a more exaggerated manner.

A
  • Classical conditioning involves pre-synaptic and post-synaptic coordination.
  • Timing is crucial in conditioning.
  • Tail shock occurs immediately after touching the siphon.
  • Pairing conditioned and unconditioned stimuli results in sensitization and habituation.
  • Both mechanisms are pre-synaptic, with sensory neurons playing a key role.
    Sensitization and Classical Conditioning Mechanisms

Sensitization:
* Facilitated interneuron releases serotonin onto sensory neuron, binds to Gs and Gq/11 pathways, activates PKA & PKC, and increases NT release and EPSP.
* Broadened Action Potential (AP) in Gs pathway due to PKA activation by cAMP from adenylyl cyclase.
* Broadened AP allows more CA2+ to enter the cell, enhancing vesicle recruitment.
* PKC phosphorylates L-type ca2+ channels, increasing vesicle recruitment and docking average number of vesicles.

Classical Conditioning:
* Sensory neuron action potential precedes shock for calmodulin to be activated, activating facilitated interneuron and serotonin release.
* Calmodulin, associated with Adenylyl cyclase, enhances Action potential and bigger PKA activation.
* Action potential in sensory neuron causes more CA2+ to enter the cell, leading to Calmodulin activation and Adenyly cyclase 4 primed, enhancing AP and bigger PKA.
* MAP K inhibits CREB 2 and activates CREB 1, directing gene transcription and PKA activation.

answer broken up on other slides as well

44
Q

Describe Classical Conditioning

A

Classical Conditioning:
* Sensory neuron action potential precedes shock for calmodulin to be activated, activating facilitated interneuron and serotonin release.
* Calmodulin, associated with Adenylyl cyclase, enhances Action potential and bigger PKA activation.
* Action potential in sensory neuron causes more CA2+ to enter the cell, leading to Calmodulin activation and Adenyly cyclase 4 primed, enhancing AP and bigger PKA.
* MAP K inhibits CREB 2 and activates CREB 1, directing gene transcription and PKA activation.

45
Q

Describe Sensitization

A

Sensitization:
* Facilitated interneuron releases serotonin onto sensory neuron, binds to Gs and Gq/11 pathways, activates PKA & PKC, and increases NT release and EPSP.
* Broadened Action Potential (AP) in Gs pathway due to PKA activation by cAMP from adenylyl cyclase.
* Broadened AP allows more CA2+ to enter the cell, enhancing vesicle recruitment.
* PKC phosphorylates L-type ca2+ channels, increasing vesicle recruitment and docking average number of vesicles.

46
Q

What is the source of inhibitory signals in central axon regeneration, and how do we know?

A

The source of inhibitory signals in central axon regeneration is the CNS myelin. We know this from past studies that were done with rats where if you block myelin sensory fibers extend normally and sprout new collaterals following denervation in myelin-free spinal cords. But if you don’t block the central axons of the branch are degenerated leaving a portion of the denervated, so little re- generation occurs in the myelin-rich cord.

47
Q

Describe the basic concept behind the synaptic tagging hypothesis.

A

The basic concept of synaptic tagging is synaptic activity “tags” a specific synapse, which essentially primes it for plasticity-induced changes. The specific tag is still unknown but multiple kinases, ion channels, and adhesion molecules have been implicated.

48
Q

Briefly explain the difference between E-LTP and L-LTP. What are the cellular events that differentiate them?

A

E- LTP is what makes the synapse more sensitive to short- term changes, the same stimulation leads to a larger response (EPSP) - PKC phosphorylates AMPA receptors, causing the insertion of AMPA receptors, then CAM
K 2 phosphorylates AMPA receptors in the membrane and sensitizes them. Result in a more robust EPSP for the same amount of stimulation. L-LTP activation of gene transcription, longer-term changes- Cam K 4 w/ MAPK phosphorylates CREB, and activation of gene transcription from early phase to late phase

49
Q

NMDA-dependent LTP and LTD can be caused by differential levels of the same type of presynaptic (non-associative) stimulation. What type of presynaptic stimulation will cause LTD instead of LTP and what differs in the mechanism to induce LTD instead of LTP (think calcium and how it activates what)?

A

Long-Term Potentiation and Long-Term Depression in NMDA Receptor-Dependent Neurons

  • Low-frequency stimulation (LFS) of presynaptic neurons, typically 1-5 Hz, is more likely to induce LTD.
  • High-frequency stimulation (HFS), typically around 100 Hz, is more likely to induce LTP.
  • LTD induction occurs when LFS results in a moderate increase in postsynaptic calcium, activating protein phosphatases and reducing the strength of the synapse.
  • LTP induction occurs when high-frequency stimulation leads to a larger calcium influx, activating calcium/calmodulin-dependent protein kinases (CaMKs), enhancing synaptic strength and promoting LTP.
  • In summary, low-frequency stimulation induces LTD, while high-frequency stimulation strengthens synapses and induces LTP.
50
Q

Describe the prototypical process of NMDA-dependent LTP. Be sure to include short-term and long-term mechanisms mediating this phenomenon

A

NMDA dependent LTP, NMDA receptor is glutamatergic and ionotropic, ion channel means it allows cations to flow through, allows Ca2+ to go through along with Na and K,
also Mg is associated with pore as negative charge to block the pore, Mg needs additional force to be ejected

51
Q

Identify the role of myelin in the regeneration of central neurons

A

Myelin forming oligodendrocytes have little or no ability to dispose of myelin, and the blood-brain barrier prevents the entry of macrophages, so removal of debris depends on a limited quantity of resident macrophages and microglia.
One is that postsynaptic injury causes axon terminals to lose their adhesiveness to synaptic sites so that they are subsequently wrapped by glia. The other is that glia initiate the process of synaptic stripping in response to factors released from the injured neuron or to changes in its cell surface.

52
Q

What is the source of inhibitory signals in central axon regeneration, and how do we know?

A

Myelin-Associated Inhibitors and Extracellular Matrix Components in the Glial Scar

Myelin-Associated Inhibitors:
* In vitro experiments show limited axon outgrowth in cultured neurons plated on myelin or myelin-derived proteins.
* Specific inhibitors like Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp) were identified.
* Antibodies or receptor blockers against these inhibitors promoted axon regeneration in animal models of spinal cord injury or optic nerve crush.

Extracellular Matrix Components in the Glial Scar:
* The glial scar contains reactive astrocytes, microglia, and a dense extracellular matrix rich in chondroitin sulfate proteoglycans (CSPGs).
* CSPGs, produced by reactive astrocytes, inhibit axon growth and regeneration.
* Treatment with chondroitinase ABC or blocking specific CSPG receptors on neurons enhanced axon regeneration

53
Q

Briefly explain the difference between E-LTP and L-LTP. What are the cellular events that differentiate them

A

Early long-term potentiation (E-LTP) is the first step of long-term potentiation (LTP). We can study the form of synaptic plasticity, and it is responsible for increase in synaptic strength.
L- Long-term potentiation (LTP) is known for continuous increase in strength of synapse by stimulating the high-frequency of chemical synapse. We can study the LTP By carrying out the hippocampus,
Cellular changes are :
LTP originates when we stimulate a single synapse repeatedly .
This event result in stimulation that causes a calcium- and CaMKII-dependent cellular cascade, which results in the insertion of more AMPA receptors which is present in synapses

54
Q

Describe the presynaptic mechanism that underlies mossy fiber LTP

A
  • LTP is a synaptic plasticity at synapses between mossy fibers and CA3 pyramidal neurons.
    It increases the probability of neurotransmitter release from mossy fibers’ presynaptic terminals.
    This increase is triggered by presynaptic calcium levels, activated by high-frequency stimulation.
    Elevated calcium levels activate signaling pathways, including CaMKII and MAPK pathways.
    These pathways phosphorylate and modulate presynaptic proteins involved in neurotransmitter release, facilitating synaptic vesicle mobilization and priming.
    Structural changes in presynaptic terminals increase the number of docked vesicles and expand the active zone area, enhancing neurotransmitter release probability.
55
Q

Describe the process of NMDA-dependent LTP. Be sure to include both short and long-term mechanisms mediating this phenomenon.

A

NMDA Receptor-Dependent Long-Term Potentiation Process
Short-Term Mechanisms:
High-frequency stimulation of presynaptic neurons initiates NMDA receptor-dependent LTP. Depolarization of the postsynaptic membrane releases Mg2+ block from NMDA receptors
Ca2+ enters postsynaptic neurons, activating calcium/calmodulin-dependent protein kinase II (CaMKII).
CaMKII phosphorylates AMPA receptors, increasing conductance and short-term synaptic response potentiation.

Long-Term Mechanisms:
* The inflow of Ca2+ activates the Ras/MAPK pathway and CaMK kinase/CaMKIV pathway, activating transcription factors like CREB.
* These transcription factors initiate the transcription of immediate early genes, leading to protein synthesis for long-term LTP maintenance.
* New proteins regulate synaptic structure and function, creating a self-perpetuating cycle of gene expression and synaptic modifications.
* These changes at the synapse underlie long-term maintenance of NMDA receptor-dependent LTP, a cellular mechanism for learning and memory formation.

56
Q

Describe the three types of LTP discussed in the hippocampus. What are they? What are the similarities and what are the differences?

A

Mossy Fiber LTP:
* Located at synapses between mossy fibers and CA3 pyramidal neurons.
* Primarily presynaptic, involving increased neurotransmitter release.
* NMDA receptor-independent, relying on presynaptic kainate receptors and cAMP signaling pathways.

Schaffer collateral LTP:
* Located at synapses between Schaffer collaterals and CA1 pyramidal neurons.
* Primarily postsynaptic, involving activation of NMDA receptors and synaptic strength increase.
* NMDA receptor-dependent, requiring large postsynaptic calcium influx.

Direct perforant path LTP:
* Located at synapses between perforant path and dentate gyrus granule cells.
* Shares similarities with both types, exhibiting both presynaptic and postsynaptic components.

Similarities:
* All three LTPs involve long-lasting synaptic strength increases and contribute to hippocampal plasticity and memory formation.
* Share common signaling pathways, including calcium involvement and kinase activation.

Differences:
* Mossy fiber LTP is primarily presynaptic and NMDA receptor-independent.
* Schaffer collateral LTP is postsynaptic and NMDA receptor-dependent.
* Direct perforant path LTP combines presynaptic and postsynaptic components.

57
Q

Hebbian or Anti-hebbian, Biased and how?

A
58
Q

Hebbian or Anti-hebbian, Biased and how?

A
59
Q

Hebbian or Anti-hebbian, Biased and how?

A
60
Q

Hebbian or Anti-hebbian, Biased and how?

A
61
Q

In the peripheral nervous system, which cells myelinate axons?
a. Microglia
b. Schwann cells
c. Oligodendrocytes
d. Astrocytes

A

b. Schwann cells

62
Q

Damage to a CNS axon leads to progressive degeneration of the distal axon as well as
a. Major downstream or postsynaptic connections
b. Major presynaptic connections
c. Myelin around the axon
d. all of the above

A

d. all of the above

63
Q

Central nervous system axons
a. Regenerate better than peripheral axons
b. Regenerate more poorly than peripheral axons
c. Regenerate quicker than peripheral axons
d. Regenerate in the opposite direction of the lesion

A

b. Regenerate more poorly than peripheral axons

64
Q

Regarding the regeneration of a damaged axon, Schwann cells
a. Prevent growth
b. Impair growth
c. Promote growth
d. Eat babies

A

Promote Growth

65
Q

What is a likely source of signals preventing central axon regeneration?
a. Schwann cells
b. Oligodendrocytes
c. Osteoblasts
d. Stem cells

A

b. Oligodendrocytes

66
Q

Which is the prototypical mechanism of degradation that results from axon injury?
a. Hebbian degeneration
b. Wallerian degeneration
c. Microglial degeneration
d. Oligodegeneratoin

A

b. Wallerian degeneration

67
Q

What functions as the coincidence detector for classical conditioning in Aplysia?
a. NMDA receptors
b. AMPA receptors
c. Adenyl Cyclase
d. Phospholipase C

A

c. Adenyl Cyclase

68
Q

Sensitization requires modification of the sensory neuron synaptic terminal by which of the following?
a. Sensory neuron
b. Motor neuron
c. Facilitating interneuron
d. Mantle

A

c. Facilitating interneuron

69
Q

Activation of PKC by the Gq pathway requires
a. Activation of Adenylyl Cyclase
b. Activation of Phospholipase C
c. Binding of glutamate
d. Action potential broadening

A

b. Activation of Phospholipase C

70
Q

Which of the following is necessary to activate PKC in Aplysia during sensitization?
a. Diacyl glycerol
b. Phosphatidyl serine
c. Phosphatidyl inositol biphosphate
d. All of the above

A

d. all of above

71
Q

Mossy fiber LTP requires activation of which:
a. NMDA receptors
b. AMPA receptors
c. PKA
d. CamKII

A

c. PKA

72
Q

Mossy fiber LTP can be induced by
a. Carefully timing presynaptic spikes with post-synaptic spikes
b. Tetanic presynaptic stimulation
c. It cant be induced
d. All of the above

A

b. Tetanic presynaptic stimulation

73
Q

Which of the following cellular processes are hypothesized to be cellular correlates of memory
a. LTP
b. LTZ
c. LTD
d. Both a and c

A

d. Both a and c

74
Q

LTP is the Schaffer collateral and the direct perforant pathway differs in the presence of which of the following mechanisms?
a. L-type calcium channel
b. Shaker potassium channels
c. Calmodulin
d. NMDA receptors

A

a. L-type calcium channel

75
Q

Which of the following is a possible condition for the induction of NMDA-dependent LTP?
a. High-frequency stimulation of presynaptic neurons
b. Low-frequency stimulation of presynaptic neurons
c. Activation of metabotropic glutamate receptors
d. None of the above

A

a. High-frequency stimulation of presynaptic neurons

76
Q

Regarding spike-timing-dependent plasticity, where cell A is presynaptic to cell B, which of the following scenarios would result in strong LTD (long-term depression)?
a. Cell B consistently firing immediately before cell A
b. Cell A consistently firing immediately before cell B
c. Cell B intermittently firing long before cell A
d. Cell A intermittently firing long before cell B

A

a. Cell B consistently firing immediately before cell A

77
Q

Regarding the binomial distribution, what changes as a result of mossy fiber LTP?
a. n
b. p
c. Q
d. X
e. None of the above

A

a. n

78
Q

Regarding the binomial distribution, what changes as a result of Schaffer Collateral LTP?
a. n
b. p
c. Q
d. X
e. None of the above

A

e. None of the above

79
Q

Phosphorylation of AMPA receptors by PKC results in
a. Insertion of new AMPA receptors into the membrane
b. Removal of AMPA receptors from the membrane
c. Insertion of NMDA receptors into the membrane
d. Inactivation of NMDA receptors

A

a. Insertion of new AMPA receptors into the membrane

80
Q

The tracing shows an EPSP induced when cell A releases glutamate onto cell B. Which of the tracings to the left represents a likely change to the EPSP after LTD had occurred?

A

B

81
Q

At resting potential, in which direction will sodium flow if an ion channel specific to it is opened?
a. Into the cell
b. Out of the cell
c. No net flow

A

a. into the cell

82
Q

At resting potential, in which direction will chloride flow if an ion channel specific to it is opened?
a. Into the cell
b. Out of cell
c. No net flow

A

into the cell

83
Q

Which ion flows with its electrical gradient?
a. Sodium
b. Potassium
c. Chloride
d. None of these

A

a. Sodium

84
Q

Which ion flows against its concentration gradient?
a. Sodium
b. Potassium
c. Calcium
d. None of the above

A

d. none of the above

maybe b. Potassium

85
Q

For an average neuron, where can an action potential be initiated?
a. Only at the axon hillock
b. Only at the axon initial segment
c. Only at the axon internodes
d. Anywhere on the neuron

A

d. anywhere on the neuron

86
Q

(Hebbian or antihebbian, and if there is a bias and what it is)

A

Hebbian LTP biased

87
Q

When studying the mechanism of hippocampal plasticity, what is commonly used for an induction protocol to ensure that LTP is induced?

A

Post tetanic potentiation

88
Q

Would the timing indicated by the III result in an increase or decrease in EPSC amplitude?

A

decrease in EPSP amplitude

89
Q

What is the frequency of this stimulation protocol?

A

10 HZ

90
Q

What is the delta t for this stimulation protocol?

A

25

91
Q

What does the z-axis represent?

A

Frequency of induction protocol

92
Q

Identify a frequency at which the synapse functions as a Hebbian

A

20 HZ

93
Q

Identify a frequency at which the synapse is LTD only

A

0.1 HZ

Development/ Plasticity (8 decks)

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