Exam 2 Flashcards

1
Q

Which type of signaling do mature neurons most commonly use to communicate?
a. Electrical only
b. Chemical only
c. A combination of electrical and chemical
d. Paracrine
e. Endocrine

A

b. chemical only

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2
Q

The effector molecule at the synapse of an intercellular signal transduction process is
a(n)
a. ion.
b. ion channel.
c. neurotransmitter molecule.
d. synaptic vesicle.
e. G-protein.

A

b. ion channel.

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3
Q
  1. What is the greatest advantage of the chemical signal transduction scheme?
    a. Signal amplification
    b. Activation of remote targets
    c. Activation of immediate targets
    d. Sequential nature
    e. Specificity
A

a. Signal amplification

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4
Q

Which molecule belongs to a class of cell-associated signaling molecules?
a. Thyroxin
b. Integrin
c. Acetylcholine
d. Testosterone
e. Nitric oxide

A

b. Integrin

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5
Q

Cell-permeant signaling molecules bind to which type of receptor?
a. Channel-linked
b. Enzyme-linked
c. G-protein–coupled
d. Intracellular
e. All of the above

A

d. Intracellular

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6
Q

Most enzyme-linked receptors affect the function of the target cell by
a. phosphorylating intracellular target proteins.
b. catalyzing synthesis of hormones in the cytoplasm.
c. facilitating the assembly of the cytoskeleton.
d. generating an action potential.
e. dimerizing.

A

a. phosphorylating intracellular target proteins.

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7
Q

To which subunit(s) of heterotrimeric G-protein does a guanine nucleotide bind?
a. α
b. β
c. βγ subunit complex
d. γ
e. δ

A

a. α

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8
Q

Which of the following is the first step in the process of activation of a heterotrimeric
G-protein?
a. The α subunit binds to β and γ subunits to form the inactive trimer.
b. The α subunit binds to GDP.
c. The G-protein binds to the activated receptor.
d. The α subunit dissociates from the βγ complex.
e. The α subunit binds to downstream effector molecules.

A

c. The G-protein binds to the activated receptor.

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9
Q

In what way does the function of monomeric G-proteins differ from that of
heterotrimeric G-proteins?
a. Monomeric G-proteins are active in the GTP-bound state, heterotrimeric G-proteins are
not.
b. Heterotrimeric G-protein activation is controlled by guanine nucleotide exchange
factors, monomeric G-protein activation is not.
c. Heterotrimeric G-proteins relay signals from cell surface receptors to intracellular
targets, monomeric G-proteins do not.

d. Monomeric G-protein activity is terminated by hydrolysis of GTP, heterotrimeric G-
protein activity is not.

e. Heterotrimeric G-protein activity is regulated by GAP proteins, monomeric G-protein
activity is not.

A

b. Heterotrimeric G-protein activation is controlled by guanine nucleotide exchange
factors, monomeric G-protein activation is not.

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10
Q

Which molecule is an effector directly downstream of an activated G-protein?
a. Phospholipase C
b. IP3
c. cAMP
d. Protein kinase C
e. Protein kinase A

A

a. Phospholipase C

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11
Q

Which role does calmodulin play in the intracellular cascade triggered by Ca2+?
a. It modulates the strength of Ca2+ binding to its downstream targets.
b. It serves as a Ca2+ buffer.
c. It enhances downstream effects of Ca2+
d. It binds to its downstream targets when activated by Ca2+
e. It serves as a Ca2+ sensor when neurotransmitter is released.

A

d. It binds to its downstream targets when activated by Ca2+

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12
Q

In which direction do Ca2+ ions flow through ryanodine receptors?
a. From the cytoplasm into the endoplasmic reticulum
b. From the endoplasmic reticulum into the cytoplasm
c. From the extracellular space into the cytoplasm
d. From the cytoplasm into the extracellular space
e. From the cytoplasm into synaptic vesicles

A

b. From the endoplasmic reticulum into the cytoplasm

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13
Q

Which second messenger originates from both extracellular and intracellular
compartments?
a. Ca2+
b. Cyclic AMP
c. Cyclic GMP
d. IP3
e. Diacylglycerol

A

a. Ca2+

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14
Q

Which second messenger plays an important role in sensory transduction processes?
a. Ca2+
b. Cyclic nucleotide
c. Nucleotide
d. IP3
e. Diacylglycerol

A

b. Cyclic nucleotide

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15
Q

Which of the following provides an example of a second messenger producing
another second messenger?
a. IP3 binds to its receptor, enabling the release of Ca2+ from the cytosol.
b. Diacylglycerol fuses with PIP2, producing IP3.
c. Phospholipase C acts on PIP2, splitting it into IP3 and diacylglycerol.
d. Ca2+ binds to calmodulin, promoting its binding to downstream protein kinases.
e. G-proteins activate adenylyl cyclase in the plasma membrane, causing it to produce
cyclic nucleotides.

A

a. IP3 binds to its receptor, enabling the release of Ca2+ from the cytosol.

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16
Q

The catalytic domain of a protein kinase
a. transfers a carboxyl group to the relevant amino acid of the target protein.
b. transfers a phosphate group to the relevant amino acid of the target protein.
c. transfers ATP to the relevant amino acid of the target protein.
d. binds to IP3
.
e. binds to Ca2+ ions.

A

b. transfers a phosphate group to the relevant amino acid of the target protein.

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17
Q
  1. Which statement about protein kinases in the brain is most accurate?
    a. They amplify second messenger signals.
    b. Most are important regulators of neuronal signaling.
    c. Each has a regulatory domain that inhibits the catalytic domain.
    d. The catalytic domain of a protein kinase is always inhibited.
    e. They can be activated only by second messengers.
A

a. They amplify second messenger signals.

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18
Q

Which protein kinase is the primary effector of cAMP?
a. PKA
b. PKC
c. CaMKII
d. Protein tyrosine kinase
e. MAPK

A

a. PKA

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19
Q

Which kinase is activated by the phosphorylation of its activation loop?
a. PKA
b. PKC
c. CaMKII
d. Protein tyrosine kinase
e. MAPK

A

c. CaMKII

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20
Q

Which statement about protein phosphatases is false?
a. They remove the phosphate group from proteins.
b. They are more specific than protein kinases with regard to substrates.
c. They possess a catalytic subunit.
d. They possess a regulatory subunit.
e. They reverse the effects of protein kinases.

A

b. They are more specific than protein kinases with regard to substrates.

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21
Q

A hallmark of Alzheimer’s disease is excessive phosphorylation of tau protein, which
is thought to be due to defects in
a. PP2A.
b. PP2B.
c. MAPK.
d. α-synuclein.
e. CaMKII.

A

a. PP2A.

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22
Q

Schizophrenia and are associated with mutations in MAOA and COMT
genes.
a. depression
b. bipolar disorder
c. panic disorder
d. generalized anxiety disorder
e. Alzheimer’s disease

A

b. bipolar disorder

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23
Q

Which of the following is the first step in the nuclear signaling process?
a. Binding of RNA polymerase
b. Binding of transcriptional activator protein
c. Binding of co-activator complex
d. Transcription
e. Chromatin decondensation

A

e. Chromatin decondensation

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24
Q

Which gene regulation strategy underlies the action of glucocorticoid hormones?
a. Translocation of the receptor into the nucleus to bind to DNA
b. DNA-bound receptor conformation change, enabling transcription
c. Phosphorylation of CREB in the nucleus
d. Activation of c-fos, an immediate early gene
e. Activation of delayed response genes

A

a. Translocation of the receptor into the nucleus to bind to DNA

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25
Q

Which neuronal mechanism increases the production of catecholamine
neurotransmitters?
a. Dimerization of tyrosine kinase receptors
b. Co-activation of metabotropic and AMPA glutamate receptors
c. Phosphorylation of tyrosine hydroxylase
d. Activation of kinases that phosphorylate CREB
e. Activation of the ras cascade

A

c. Phosphorylation of tyrosine hydroxylase

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26
Q

Which signaling molecule mediates nerve growth factor (NGF)-dependent neuronal
survival?
a. Akt kinase
b. IP3
c. DAG
d. MAPK
e. Ras

A

a. Akt kinase

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27
Q

What are some potential points of intersection (molecules) between second messenger
systems?

A

CREB, kinases, second messengers, G-proteins

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28
Q

How do second messenger systems “turn off” after they have been turned on?

A

Enzymes such as phosphatases and phosphodiesterases facilitate turning off of
second messenger cascades.

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29
Q

Define and provide an example of each of the following:
Cell signaling molecules
Receptors
G-proteins
Effector proteins
Second messengers
Later effectors
Transcription factors
Immediate early genes

A

Cell signaling molecules: Molecules that activate intracellular signaling pathways.
Examples: neurotransmitters, hormones, integrins
Receptors: Molecules that bind to signaling molecules specifically. Examples: nicotinic
acetylcholine receptor, metabotropic glutamate receptor
G-proteins: Molecules that couple receptors and their downstream effectors. Examples:
GS, Gq
Effector proteins: Molecules that serve as downstream targets of G-proteins. Example:
adenylyl cyclase
Second messengers: Products of effector proteins. Examples: cAMP, IP3, Ca2+
Later effectors: Targets of second messengers, typically, protein kinase enzymes that
phosphorylate their molecular targets. Examples: protein kinase A, protein kinase C
Transcription factors: Proteins that regulate the transcription process. Example: CREB
Immediate early genes: Genes that are expressed immediately after cell stimulation; their
products act as transcription factors for delayed response genes. Example: c-fos

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30
Q

Why is it crucial that Ca2+ levels are maintained at low concentrations inside the cell?
What is the mechanism of action that maintains a low concentration?

A

Ca2+ is a second messenger, and increases in its intracellular concentration can
trigger signaling cascades and other events inside the cell. Pumping of Ca2+ into the
intracellular compartments and extracellular space maintains low levels of Ca2+ levels.

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31
Q

Which pathway(s) can be activated by nerve growth factor (NGF)? What are some of
the diverse effects of NGF?

A

The PI3 kinase pathway, ras pathway, and phospholipase C pathway are all
activated by NGF. NGF mediates neuronal survival, neurite outgrowth, and neuronal
differentiation.

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32
Q

Which type of chemical signaling acts over a small neural region encompassing a
cluster of nerve cells?
a. Endocrine
b. Exocrine
c. Paracrine
d. Synaptic
e. Ephaptic

A

c. Paracrine

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33
Q

In a signal transduction cascade using G-proteins and cAMP, which is not a signal
amplification step?
a. Activation of G-proteins by an activated receptor
b. Activation of adenylyl cyclase molecules by G-proteins
c. Creation of cAMP molecules by adenylyl cyclase
d. Phosphorylation of target proteins by protein kinase A
e. All of the above are steps in which amplification occurs

A

b. Activation of adenylyl cyclase molecules by G-proteins

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34
Q

Which statement about cell signaling pathways is true?
a. Cellular responses are always short-lived.
b. Cellular responses are always long-lived.
c. Signaling is always initiated by membrane-bound receptors.
d. Signaling is always initiated by intracellular receptors.
e. Intracellular signal transduction pathways are always activated by a chemical signaling
molecule.

A

e. Intracellular signal transduction pathways are always activated by a chemical signaling
molecule.

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35
Q

The acetylcholine receptor at the neuromuscular junction would best be described as
a(n)
a. channel-linked receptor.
b. enzyme-linked receptor.
c. G-protein-coupled receptor.
d. nuclear receptor.
e. gap junction.

A

a. channel-linked receptor.

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36
Q

Cholera toxin locks the Gs subunit into an active state, in that GTP is bound and cannot
be hydrolyzed back to GDP to turn off the subunit. What effect will cholera toxin have in
the cell?
a. The Gs subunit will more strongly inhibit adenylyl cyclase.
b. Inhibited adenylyl cyclase will lead to increased cyclic AMP levels.
c. Activated adenylyl cyclase will lead to decreased cyclic AMP levels.
d. Increased cyclic AMP levels will lead to increased protein kinase A activation.
e. Decreased cyclic AMP levels will lead to decreased protein kinase A activation.

A

d. Increased cyclic AMP levels will lead to increased protein kinase A activation.

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37
Q

In the marine mollusk, Aplysia, serotonin binds to a G-protein-coupled receptor and
activates a Gs subunit. The resulting activation of PKA leads to phosphorylation and
closure of K+channels. What effect would this have on the cell?

a. Decreased K+efflux depolarizing the cell

b. Increased K+efflux hyperpolarizing the cell

c. Decreased K+efflux hyperpolarizing the cell

d. Increased K+efflux depolarizing the cell

e. No change in K+
ion flow or membrane potential

A

a. Decreased K+efflux depolarizing the cell

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38
Q

Stimulation of metabotropic receptors cannot
a. open ion pores in the G-protein structure.
b. cause G-proteins to alter ion channels.
c. cause G-proteins to start second messenger cascades.
d. lead to widespread protein phosphorylation.
e. lead to gene transcription.

A

a. open ion pores in the G-protein structure.

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39
Q

Which of the following does not contribute to maintaining low levels of calcium in
resting nerve cells?
a. Voltage-gated calcium channels
b. The plasma membrane calcium ATPase
c. The smooth endoplasmic reticulum calcium ATPase
d. The Na+/ Ca2+ calcium exchanger
e. Mitochondria

A

a. Voltage-gated calcium channels

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40
Q

Which substance is a second messenger whose activity is terminated by a phosphatase?
a. Calcium
b. CAMP
c. cGMP
d. Inositol trisphosphate
e. Diacylglycerol

A

d. Inositol trisphosphate

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41
Q

Which signaling pathway does not directly involve calcium?
a. Ryanodine receptor
b. IP3 receptor
c. cGMP
d. Phospholipase C
e. Calmodulin

A

c. cGMP

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42
Q

Which development (by Tsien and colleagues) enabled the first precise spatial and
temporal measurements of intracellular calcium dynamics?
a. Voltage clamp
b. Fura-2
c. Calcium green
d. GFP
e. Channel rhodopsin

A

b. Fura-2

43
Q

Which statement about protein kinase-based signaling is false?
a. Serine and threonine kinases are typically activated by second messengers.
b. Tyrosine kinases are typically activated by extracellular signals.
c. Each protein kinase has just one specific target protein that it phosphorylates.
d. The effects of protein kinases can be balanced by protein phosphatases.
e. Thousands of protein kinases are expressed in the brain.

A

c. Each protein kinase has just one specific target protein that it phosphorylates.

44
Q

Which kinase is activated (in part) by a lipid?
a. Protein kinase A
b. Protein kinase C
c. Protein kinase G
d. CaM kinase II
e. CaM kinase IV

A

b. Protein kinase C

45
Q

Which of the following is not integral to the functioning of protein kinases?
a. Hydrolysis of GTP prior to association of the regulatory and catalytic domains
b. Reliance on functionally distinct roles of the different domains
c. Binding of one or more messengers to a regulatory domain
d. Inhibition of a catalytic domain by a regulatory domain
e. Activation of a catalytic domain via a protein conformational change

A

a. Hydrolysis of GTP prior to association of the regulatory and catalytic domains

46
Q

Dendritic spines
a. were discovered with the invention of electron microscopy in the 1950s.
b. serve as “electrical compartments” to ensure localized depolarization.
c. serve as “chemical compartments” to concentrate biochemical mechanisms.
d. collectively form a set of hard-wired permanent neural connections.
e. are the sites of all excitatory and inhibitory synaptic transmission in the mammalian
CNS.

A

c. serve as “chemical compartments” to concentrate biochemical mechanisms.

47
Q

Which statement about dendritic spines is false?
a. They enable localized, transient increases in calcium.
b. They slow the diffusion of IP3, but do not prevent it from leaving the spine.
c. They are the sites of excitatory synapses in various parts of the CNS.
d. They have a bulbous head connected to a dendritic shaft by a narrow neck.
e. They usually contain just three proteins: NMDA receptors, mGluR receptors, and CaM
kinase II.

A

e. They usually contain just three proteins: NMDA receptors, mGluR receptors, and CaM
kinase II.

48
Q

Which chemical signaling process is the slowest?
a. Ion channel-mediated depolarization
b. G-protein-mediated modulation of ion channels
c. Phosphorylation of effector molecules by protein kinases
d. Synthesis of proteins after CREB activation
e. All of the above types of signaling processes have similar time courses

A

d. Synthesis of proteins after CREB activation

49
Q

Listed below are the events that make up NGF-mediated growth of sensory neurons.
1. TrkA receptor self-phosphorylation
2. Translocation of activated kinases to the nucleus
3. NGF-induced dimerization of membrane receptors
4. TrkA induction of the ras signaling pathway
Which is the correct sequence of these events?
a. 1; 4; 3; 2
b. 4; 1; 3; 2
c. 3; 4; 1; 2
d. 3; 1; 4; 2
e. 1; 3; 4; 2

A

d. 3; 1; 4; 2

50
Q

Which statement about the LTD mechanism in cerebellar Purkinje cells is false?
a. Alternating activation of climbing fibers and parallel fibers is required to induce LTD.
b. The firing of parallel fibers activates mGluR receptors and generates IP3.
c. Climbing fibers generate a large calcium signal in Purkinje cell dendrites.
d. Both IP3 and calcium are required to activate the IP3 receptors and depress AMPA
receptor activity.
e. The strength of the parallel fiber synapses can be depressed for a long period of time.

A

a. Alternating activation of climbing fibers and parallel fibers is required to induce LTD.

51
Q

Tyrosine hydroxylase is a substrate for which protein kinase(s)?
a. PKA
b. PKC
c. CaM kinase II
d. MAP kinase
e. All of the above

A

e. All of the above

52
Q

What causes synaptic facilitation?
a. Buildup of Ca2+ in the presynaptic terminal
b. Release of greater than usual number of synaptic vesicles
c. Release of synaptic vesicles loaded with extra neurotransmitter
d. Activation of synaptotagmin 7 by means of phosphorylation
e. Stronger binding of Ca2+ to synaptotagmin 7

A

a. Buildup of Ca2+ in the presynaptic terminal

53
Q

How would an increase in external Ca2+ concentration affect synaptic depression?
a. It would increase the rate of depression.
b. It would reduce the rate of depression.
c. It would decrease the rate of neurotransmitter release and induce depression.
d. It would increase the rate of neurotransmitter release and delay depression.
e. It would have no effect on depression.

A

a. It would increase the rate of depression.

54
Q

Which type of short-term synaptic plasticity lasts the longest?
a. Potentiation
b. Augmentation
c. Depression
d. Facilitation
e. Post-tetanic potentiation

A

e. Post-tetanic potentiation

55
Q

What characteristic(s) make(s) Aplysia californica a practical model organism for
studying the nervous system?
a. Its great magnitude and variety of neurons
b. Its large neurons
c. The random location of its neurons
d. That it is aquatic
e. All of the above

A

b. Its large neurons

56
Q

Repeated stimulation of the siphon results in habituation. Which synaptic change occurs
during habituation?
a. The synapse between the sensory and motor neurons is depressed.
b. The synapse between the sensory and motor neurons is potentiated.
c. The synapse between the sensory neuron and the interneuron is depressed.
d. The synapse between the sensory neuron and the modulatory interneuron is depressed.
e. The synapse between the interneuron and the motor neuron is depressed.

A

a. The synapse between the sensory and motor neurons is depressed.

57
Q

The function of which synapse is altered during sensitization?
a. The synapse between the sensory neuron of the siphon and the motor neuron
b. The synapse between the sensory neuron of the tail and the modulatory interneuron
c. The synapse between the sensory neuron of the siphon and the interneuron
d. The synapse between the interneuron and the motor neuron
e. The synapse between the modulatory interneuron and sensory neuron of the siphon

A

a. The synapse between the sensory neuron of the siphon and the motor neuron

58
Q

Complete the sequence of events that take place in the presynaptic enhancement
underlying short-term behavioral sensitization: Serotonin is released from facilitatory
interneuron; Ca2+ influx into the presynaptic terminal is enhanced; more neurotransmitter
is released; synaptic transmission is enhanced
a. IP3 signaling keeps postsynaptic K+
channels closed.

b. IP3 signaling keeps presynaptic K+
channels closed.

c. PKA signaling keeps presynaptic K+
channels closed.

d. PKA signaling keeps presynaptic K+
channels open.

e. cAMP signaling keeps presynaptic K+
channels open.

A

c. PKA signaling keeps presynaptic K+
channels closed.

59
Q

Which process differentiates long-term from short-term sensitization?
a. Synaptic transmission between the facilitatory and sensory neurons
b. Changes in gene expression
c. PKA activation
d. Production of cAMP
e. Changes in the synapses between the sensory and motor neurons

A

b. Changes in gene expression

60
Q

Which characteristic of a living hippocampus slice is critically important to its
suitability as an experimental system for studying learning?
a. Its architecture: the hippocampus can be sectioned without destroying relevant circuits.
b. The hippocampus contains few neurons, which makes it easy to study.
c. The layer of the pyramidal neurons is divided into several regions.
d. Long-term potentiation takes place in hippocampal synapses.
e. The hippocampus is involved in learning.

A

a. Its architecture: the hippocampus can be sectioned without destroying relevant circuits.

61
Q

LTP represents a lasting increase in the size of EPSP
a. following a high-frequency train of stimuli.
b. following a low-frequency train of stimuli.
c. following a single stimulus.
d. that is restricted to the hippocampus.
e. that is restricted to the cortex.

A

a. following a high-frequency train of stimuli.

62
Q

Which property of LTP underlies Pavlovian conditioning?
a. Requirement for coincident activation of pre- and postsynaptic neurons
b. Specificity of input
c. Associativity
d. Complementarity
e. Transience

A

c. Associativity

63
Q

Which condition(s) must be met to induce LTP?
a. Glutamate must be released from the presynaptic terminal.
b. Glutamate must open the postsynaptic AMPA receptors.
c. The postsynaptic membrane must be depolarized for a period of time.
d. Mg2+ block must be expelled from NMDA receptors to allow Ca2+ influx.
e. All of the above

A

e. All of the above

64
Q

What is the immediate consequence of Mg2+ blockade removal from the NMDA
receptors?
a. Ca2+ influx into the presynaptic terminal
b. Ca2+ influx into the postsynaptic terminal
c. Na+influx into the postsynaptic terminal
d. Postsynaptic EPSP
e. Glutamate binding to its receptors

A

b. Ca2+ influx into the postsynaptic terminal

65
Q

What would happen if Mg2+ was not expelled from NMDA channels?
a. Glutamate would not bind to NMDA receptors.
b. Glutamate would not bind to AMPA receptors.
c. The postsynaptic membrane would not depolarize.
d. EPSP would not occur.
e. LTP would not occur.

A

e. LTP would not occur.

66
Q

What is the mechanism of LTP expression?
a. Increase in the number of postsynaptic NMDA receptors
b. Increase in the number of postsynaptic AMPA receptors
c. Increase in the number of presynaptic AMPA receptors
d. Increase in the intracellular level of synaptotagmins
e. Decrease in the level of glutamate released into the synaptic cleft

A

b. Increase in the number of postsynaptic AMPA receptors

67
Q

Which protein facilitates the late phase of LTP?
a. Synaptotagmin
b. CaMKII
c. CREB
d. PKC
e. Clathrin

A

c. CREB

68
Q

Which process does not take place during LTD?
a. Activation of protein kinases
b. Activation of protein phosphatases
c. Activation of PKC
d. Activation of clathrin
e. Activation of synaptotagmin

A

a. Activation of protein kinases

69
Q

Which second messenger(s) is(are) involved in postsynaptic depression?
a. Ca2+ only
b. cAMP and Ca2+ only
c. DAG and IP3 only
d. Ca2+, DAG, and IP3
e. cAMP, Ca2+, DAG, and IP3

A

d. Ca2+, DAG, and IP3

70
Q

Which statement about silent synapses is true?
a. They cannot be induced to transmit information.
b. They transmit information at a resting membrane potential.
c. They can produce postsynaptic responses as a result of LTP.
d. They contain both NMDA and AMPA receptors.
e. They represent mature glutamatergic synapses.

A

b. They transmit information at a resting membrane potential.

71
Q

What triggers LTD?
a. Ca2+ influx into the postsynaptic terminal
b. Internalization of AMPA receptors
c. High-frequency stimulation
d. Low-frequency stimulation followed by small or slow increase in Ca2+
e. Low-frequency stimulation followed by sharp and dramatic increase in Ca2+

A

d. Low-frequency stimulation followed by small or slow increase in Ca2+

72
Q

At which time interval between pre- and postsynaptic activity would STDP occur?
a. 20 ms, but only if presynaptic activity occurs before postsynaptic activity
b. 30 ms, but only if postsynaptic activity occurs before presynaptic activity
c. 40 ms, regardless of whether pre- or postsynaptic activity occurs first
d. 10–100 ms, regardless of whether pre- or postsynaptic activity occurs first
e. 40–100 ms, regardless of whether pre- or postsynaptic activity occurs first

A

c. 40 ms, regardless of whether pre- or postsynaptic activity occurs first

73
Q

Which statement about kindling is true?
a. Its effect is reversible.
b. Its effect is long-lasting.
c. It is based on use of a single, weak stimulus to change the excitability of the brain.
d. It is used to treat epilepsy.
e. It is used to diagnose epilepsy.

A

b. Its effect is long-lasting.

74
Q

Define the term “synaptic plasticity.”

A

It is the ability of synapses to change in strength.

75
Q

How do the short-term forms of synaptic plasticity contribute to learning and memory?

A

They cause the transmission at chemical synapses to change dynamically as a
consequence of the recent history of synaptic activity, that is, experience.

76
Q

What is the synaptic basis for short-term sensitization in Aplysia?

A

Modulatory interneurons strengthen synaptic transmission in the gill withdrawal
circuit, that is, the synapses between the sensory and motor neurons of the siphon.

77
Q

Define long-term potentiation (LTP). Draw a diagram that shows how LTP is obtained
experimentally in CA1 of the hippocampus.

A

Long-term potentiation represents a long-lasting increase in synaptic strength.

78
Q

What is needed for: a) the initial acquisition of LTP and b) the maintenance of long-
lasting LTP?

A

a) Increase in postsynaptic Ca2+
b) Increase in the number of postsynaptic AMPA receptors with subsequent changes in
protein expression in the postsynaptic cell

79
Q

What is long-term depression (LTD)? How is it produced experimentally?

A

Long-term depression is a persistent, activity-dependent weakening of synaptic
transmission. It can be produced in the lab by stimulating Schaffer collaterals at a low
frequency/rate for a long period of time /10–15 minutes.

80
Q

Compare cellular mechanisms involved in LTP versus LTD.

A

LTP is accompanied by an increase in the number of postsynaptic AMPA
receptors, whereas LTD is accompanied by a decrease in the number of postsynaptic
AMPA receptors.

81
Q

How are silent synapses converted to active excitatory synapses?

A

Silent synapses are turned “on” when (induced by LTP) AMPA receptors are
added to postsynaptic membranes, and the postsynaptic cell becomes responsive to
glutamate.

82
Q

Why is it thought that Ca2+ levels might be involved in spike timing-dependent
plasticity (STDP)?

A

If postsynaptic Ca2+ levels are high (as they are when presynaptic activity
precedes postsynaptic potential), LTP occurs. If postsynaptic Ca2+levels are low (as they are when postsynaptic potential precedes presynaptic activity), LTD occurs.

83
Q

What might LTP and epilepsy have in common?

A

Long-lasting or even permanent changes in neuronal circuitry underlie both LTP
and epilepsy.

84
Q

Which statement about the plasticity of synapses in the mammalian CNS is false?
a. The hallmark of both short-term and long-term synaptic plasticity is that they always
increase the strength of synaptic connections.
b. The efficacy of synapses can be adjusted by modulating the amount of
neurotransmitter that is released.
c. Calcium ions play a central role in at least some forms of synaptic plasticity.
d. Changes in synaptic efficacy can occur over time scales ranging from milliseconds to
years.
e. A variety of molecular mechanisms are involved in the different forms of synaptic
plasticity.

A

a. The hallmark of both short-term and long-term synaptic plasticity is that they always
increase the strength of synaptic connections.

85
Q

Firing an action potential in an axon initially causes a 10-mV depolarization (EPSP) in
a postsynaptic neuron, but after applying a certain stimulus to the axon, firing it causes an
8-mV depolarization after each action potential. This phenomenon is called synaptic
a. enhancement.
b. depression.
c. facilitation.
d. augmentation.
e. potentiation.

A

b. depression.

86
Q

After firing a short burst of action potentials in an axon, researchers observe a larger
EPSP in the postsynaptic cell, and this effect seems to last a few tens of milliseconds.
This is most likely due to the presynaptic terminal having
a. extra calcium.
b. lowered calcium.
c. extra sodium.
d. reduced sodium.
e. extra magnesium.

A

a. extra calcium.

87
Q

Which mechanism would be a plausible explanation for synaptic depression?
a. Inhibition of postsynaptic calcium channels
b. Activation of presynaptic potassium channels
c. Depletion of docked synaptic vesicles in the presynaptic terminal
d. Faster replenishment of vesicles to the reserve pool
e. Enhancement of presynaptic sodium currents

A

c. Depletion of docked synaptic vesicles in the presynaptic terminal

88
Q

Which statement about long-term synaptic plasticity is false?
a. The efficacy of transmission at many synapses depends on their history of synaptic
activity.
b. The tracking of long-term changes in synaptic efficacy is difficult in mammalian
systems because of the complexity of mammalian brains.
c. The gill withdrawal reflex in Aplysia can be enhanced by pairing a noxious stimulus
with a mild touch.
d. Associative learning in the Aplysia gill withdrawal reflex is relatively independent of
the timing or the order in which different stimuli are applied.
e. Gill withdrawal behavior in Aplysia can be altered for days or weeks by means of
repeated pairings of shocks and touches.

A

d. Associative learning in the Aplysia gill withdrawal reflex is relatively independent of
the timing or the order in which different stimuli are applied.

89
Q

Which mechanism contributes to the long-term enhancement of the gill withdrawal
reflex in Aplysia but is not involved in the short-term enhancement of the reflex?
a. Activation of G-protein-coupled receptors by serotonin
b. Phosphorylation of CREB
c. Activation of adenylyl cyclase
d. Activation of protein kinase A
e. Decreased opening of potassium channels during presynaptic action potentials

A

b. Phosphorylation of CREB

90
Q

Learning and memory processes in the fruit fly Drosophila show striking molecular
overlap with analogous processes in Aplysia, in terms of their using all of the following
except
a. phosphodiesterase.
b. adenylyl cyclase.
c. adenylyl cyclase activating pathways.
d. allosteric modulation of GABA receptors.
e. CREB gene regulation.

A

d. allosteric modulation of GABA receptors.

91
Q

Which statement about LTP is false?
a. LTP involves an enhancement in synaptic efficacy that can last for hours, days, weeks
or even longer.
b. If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and another
nearby synapse (B) on the same dendrite is weakly stimulated at the same time, then the
second synapse (B) will also show LTP.
c. If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and a nearby
synapse (B) on the same cell is weakly stimulated a few seconds later, then the second
synapse (B) will also show LTP.
d. The requirement for coincident pre- and postsynaptic activity was predicted by Donald
Hebb in 1949.
e. Hippocampal LTP was first reported by Bliss and Lomo about 1970.

A

c. If one synapse (A) is very strongly stimulated (sufficient to cause LTP), and a nearby
synapse (B) on the same cell is weakly stimulated a few seconds later, then the second
synapse (B) will also show LTP.

92
Q

An electrode is used to stimulate a presynaptic nerve that synapses in the dentate
gyrus (DG) of the hippocampus. Postsynaptic recordings are measured in the DG
neurons. First a weak stimulus (stimulus A) is applied, and then a strong stimulus
(stimulus B). If a second weak stimulus (stimulus C) is applied after the strong
stimulus, which result would you expect?
a. The postsynaptic response to the second weak stimulus (C) will be higher than the
response to the strong stimulus (B).
b. The postsynaptic response to the second weak stimulus (C) will be lower than the
response to the first weak stimulus (A).
c. The postsynaptic response to the second weak stimulus (C) will be equal to the
response to the first weak stimulus (A).
d. The postsynaptic response to the second weak stimulus (C) will be equal to the
response to the strong stimulus (B).
e. The postsynaptic response to the second weak stimulus (C) will be higher than the
response to the first weak stimulus (A).

A

e. The postsynaptic response to the second weak stimulus (C) will be higher than the
response to the first weak stimulus (A).

93
Q

A researcher is trying to study synaptic transmission in a glutamatergic
hippocampal neuron. She is tasked with measuring calcium flow in the postsynaptic
hippocampal neuron after either low or high intensity stimulation to the presynaptic
neuron. During the experiment, she measures calcium influx after both low and high
stimulation. Which statement best describes the error she made?
a. She forgot to add magnesium to the extracellular solution
b. She forgot to add calcium to the extracellular solution
c. She forgot to add sodium to the extracellular solution
d. She forgot to add potassium to the extracellular solution
e. She completed all steps correctly.

A

a. She forgot to add magnesium to the extracellular solution

94
Q

You are examining long-term potentiation in two groups of hippocampal neurons:
control and treated. You induce lasting LTP in the control cells after repetitive high-
frequency stimulation. In the treated cell, however, the potentiation begins to decrease
after 2 hours. What treatment was given?
a. A drug that blocks sodium channels
b. A drug that opens calcium channels
c. A drug that binds magnesium
d. A drug that inhibits protein synthesis
e. A drug that blocks clathrin

A

d. A drug that inhibits protein synthesis

95
Q

The type of receptor that is critical for the induction of hippocampal LTP, admitting
calcium into a dendritic spine, is called a(n)
a. AMPA receptor.
b. NMDA receptor.
c. glycine receptor.
d. cholinergic GPCR.
e. noradrenergic GPCR.

A

b. NMDA receptor.

96
Q

The key aspect of receptor-gating in the associative induction of hippocampal LTP is
that
a. all glutamate receptors open automatically whenever glutamate is in the synaptic cleft.
b. the NMDA receptor acts as a molecular coincidence detector.
c. the AMPA receptor allows calcium into the cell only after the NMDA receptor is
activated.
d. both the NMDA and AMPA channels must be open in order for the cell to depolarize.
e. The NMDA receptor allows the flow of magnesium into the cell.

A

b. the NMDA receptor acts as a molecular coincidence detector.

97
Q

Which statement about the mechanisms underlying hippocampal LTP induction is
false?
a. An influx of calcium triggers two or more intracellular processes in the postsynaptic
dendritic spine.
b. Calcium may enhance transmitter release from the presynaptic terminal.
c. Calcium may activate Ca2+/calmodulin-dependent protein kinase type II (CaMKII),
which then autophosphorylates, leading to a long-term “on” state.
d. Calcium may activate a signaling cascade that causes the insertion of glutamate
receptors into the postsynaptic membrane.
e. Calcium decreases a resting leak current of sodium so that the postsynaptic cell is
closer to threshold and therefore fires more easily.

A

e. Calcium decreases a resting leak current of sodium so that the postsynaptic cell is
closer to threshold and therefore fires more easily.

98
Q

Silent synapses are “silent” because they
a. have no presynaptic terminal.
b. have AMPA receptors but no NMDA receptors.
c. have NMDA receptors but no AMPA receptors.
d. lack voltage-gated sodium channels.
e. are continuously inhibited and so cannot be activated.

A

c. have NMDA receptors but no AMPA receptors.

99
Q

Which mechanism used in hippocampal LTD is not part of the hippocampal LTP
mechanism?
a. History-dependent modification of synaptic efficacy
b. NMDA receptor activation
c. Calcium influx
d. Calcium-dependent activation of protein phosphatases
e. Calcium-dependent activation of protein kinases.

A

d. Calcium-dependent activation of protein phosphatases

100
Q

The targets of the phosphatases activated during hippocampal LTD are
a. voltage-gated ion channels.
b. ligand-gated ion channels.
c. synaptic vesicle regulatory proteins.
d. postsynaptic signaling pathways.
e. unknown.

A

e. unknown.

101
Q

Cerebellar LTD depends on
a. synergistic actions of calcium and IP3 on internal calcium release channels.
b. synergistic actions of sodium and IP3 on internal calcium release channels.
c. activation of AMPA receptors by voltage-gated ion channels.
d. binding of IP3 to clathrin to activate endocytosis.
e. calcium-dependent insertion of GABA receptors into the postsynaptic membrane.

A

a. synergistic actions of calcium and IP3 on internal calcium release channels.

102
Q

Which observation would demonstrate the spike timing-dependent plasticity of
synapses?
a. Whether or not LTP occurs is dependent on the specific temporal pattern of action
potentials.
b. LTP occurs whenever an action potential precedes an EPSP.
c. LTD occurs whenever an action potential follows an EPSP.
d. Switching the relative timing of action potential and EPSP by as little as 20 ms can
switch the response from LTD to LTP, or vice-versa.
e. A rhythmic pattern of spike–EPSP–spike–EPSP, at 40 ms intervals, produces maximal
LTP.

A

d. Switching the relative timing of action potential and EPSP by as little as 20 ms can
switch the response from LTD to LTP, or vice-versa.

103
Q

In the context of neuropathological activity, the phenomenon of kindling refers to
a. small burns made in cortex by an electrical stimulating electrode.
b. the ability to induce LTP in the amygdala and other brain regions in live animals.
c. the ability of daily administration of a weak, low-amplitude train of electrical pulses to
gradually evoke larger and larger behavioral responses.
d. the phenomenon whereby a single, strong electrical pulse can evoke a full-blown
seizure.
e. chaotic patterns of neural activity resembling the flame of a candle.

A

c. the ability of daily administration of a weak, low-amplitude train of electrical pulses to
gradually evoke larger and larger behavioral responses.