Deck 11: Mechanisms of Direct Synaptic Transmission

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Question
How does information transfer occur at electrical synapses?

A) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through connexons (or gap junctions).
B) Electrical depolarization of the nerve terminal causes presynaptic calcium channels to open, leading to the direct excitation of the postsynaptic cell.
C) Electrical depolarization of the nerve terminal causes the release of chemicals that open postsynaptic ligand-gated ion channels which pass current, depolarizing the postsynaptic cell.
D) Electrical depolarization of the nerve terminal directly opens postsynaptic ligand-gated ion channels, which pass current, depolarizing the postsynaptic cell.
E) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through voltage-gated ion channels.
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Question
How does information transfer occur at chemical synapses?

A) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through connexons (or gap junctions).
B) Electrical depolarization of the nerve terminal causes presynaptic calcium channels to open, leading to the direct excitation of the postsynaptic cell.
C) Electrical depolarization of the nerve terminal causes the release of chemicals that open postsynaptic ligand-gated ion channels which pass current, depolarizing the postsynaptic cell.
D) Electrical depolarization of the nerve terminal directly opens postsynaptic ligand-gated ion channels, which pass current, depolarizing the postsynaptic cell.
E) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through voltage-gated ion channels.
Question
Following years of debate about chemical vs. electrical transmission at synapses in the brain, which form of transmission was found to exist?

A) All neurons in the brain were found to use electrical transmission.
B) All neurons in the brain were found to use chemical transmission.
C) Some neurons in the brain were found to use electrical transmission, others chemical transmission, and some both forms of transmission.
D) All neurons in the brain were found to initially use chemical transmission, and then convert to electrical transmission.
E) All neurons in the brain were found to initially use electrical transmission, and then convert to chemical transmission.
Question
Dendritic spines are commonly a site for

A) both excitatory and inhibitory synaptic transmission.
B) inhibitory synaptic transmission.
C) excitatory synaptic transmission.
D) storage of transmitter molecules.
E) active zones.
Question
Which of the following does not exist at a direct chemical synapse?

A) Synaptic vesicles
B) 30 nm synaptic cleft
C) Postsynaptic ligand gated ion channel receptors
D) Connexon proteins (gap junctions)
E) Active zones
Question
What is the "synaptic cleft"?

A) The nerve terminal
B) The postsynaptic collection of receptors
C) The space between the presynaptic neuron and the postsynaptic cell
D) The postsynaptic change in membrane potential
E) The active zone
Question
At the NMJ, postjunctional folds radiate into the muscle fiber from the cleft at
Regular intervals. What is their role at neuromuscular synapses?

A) Binding transmitter molecules
B) Increasing the postsynaptic surface area for receptors
C) Reducing the space between the presynaptic and postsynaptic cells
D) Increasing the space between presynaptic and postsynaptic cells
E) Degrading transmitter after binding to receptors
Question
How does acetycholinesterase function at synapses that release acetylcholine?

A) It is a postsynaptic muscarinic receptor blocker.
B) It is a postsynaptic nicotinic receptor blocker.
C) It is a synaptic cleft enzyme that breaks down acetylcholine receptor proteins.
D) It is a presynaptic calcium channel agonist.
E) It is a synaptic cleft enzyme that breaks down the transmitter acetylcholine.
Question
How do transmitters act on the postsynaptic cell at direct chemical synapses?

A) They diffuse across postsynaptic membranes to excite postsynaptic cells.
B) They bind to voltage-gated ion channels to induce postsynaptic current flux.
C) They bind to metabotropic receptors to induce postsynaptic biochemical changes.
D) They bind to ligand-gated ion channels to induce postsynaptic current flux.
E) They bind to extracellular matrix molecules to excite postsynaptic cells.
Question
Synaptic vesicles are concentrated in large numbers within nerve terminals. What is their function?

A) They have no known function.
B) They engulf foreign proteins for degradation.
C) They fuse with mitochondria to transport ATP.
D) They store and deliver active zone proteins to the plasma membrane.
E) They store and release chemical transmitter molecules.
Question
What is an endplate potential?

A) The membrane potential that a nerve terminal will release transmitter.
B) The membrane potential that a postsynaptic muscle cell will reach threshold.
C) Depolarization of the endplate region of the muscle fiber following acetylcholine binding to postsynaptic nicotinic acetylcholine receptors.
D) Hyperpolarization of the endplate region of the muscle fiber following acetylcholine binding to postsynaptic nicotinic acetylcholine receptors.
E) Depolarization of the endplate region of the muscle fiber following acetylcholine binding to muscarinic receptors.
Question
How does the size and shape of the endplate potential change when recorded at different distances from the endplate at the NMJ?

A) The EPP does not change when recorded at different distances from the NMJ.
B) The EPP has the same amplitude but has a slower time course when recorded at increasing distances from the NMJ.
C) The EPP has reduced amplitude but the same time course when recorded at increasing distances from the NMJ.
D) The EPP has both a reduced amplitude and slower time course when recorded at increasing distances from the NMJ.
E) The EPP has both an increased amplitude and slower time course when recorded at increasing distances from the NMJ.
Question
An inhibitory postsynaptic potential (IPSP) occurs when

A) the ligand-gated ion channels with a reversal potential that is more negative than membrane potential open in the postsynaptic membrane in response to transmitter binding.
B) the ligand-gated ion channels with a reversal potential that is more positive than membrane potential open in the postsynaptic membrane in response to transmitter binding.
C) metabotropic receptors are activated by transmitter binding.
D) voltage-gated ion channels open during an action potential.
E) the ligand-gated ion channels without a reversal potential open in the postsynaptic membrane in response to transmitter binding.
Question
Why does the plant alkaloid nicotine cause skeletal muscle contraction?

A) Nicotine causes presynaptic action potentials.
B) Nicotine blocks postsynaptic nicotinic acetylcholine receptors.
C) Nicotine is an agonist at postsynaptic muscarinic acetylcholine receptors.
D) Nicotine is an agonist at postsynaptic nicotinic acetylcholine receptors.
E) Nicotine increases presynaptic calcium channel function, increasing transmitter release.
Question
How do acetycholinesterase drugs (i.e. physostigmine) alter EPPs?

A) Physostigmine prolongs the time course of EPPs.
B) Physostigmine blocks EPPs.
C) Physostigmine shortens the time course of EPPs.
D) Physostigmine has no effect on EPPs.
E) Physostigmine prevents the transmitter release that causes EPPs.
Question
What determines the decay time for an endplate potential?

A) The time course of acetylcholine release from the nerve terminal
B) The time that acetylcholine is present in the synaptic cleft
C) The time constant of the presynaptic nerve cell membrane
D) The mean open time of the acetylcholine receptor channel
E) The time constant of the muscle fiber membrane
Question
What is the subunit composition of the NMDA receptor?

A) Four GluN1 subunits arranged as a tetramer
B) Four GluN2 subunits arranged as a tetramer
C) Two GluN1 subunits and three GluN2 subunits, arranged as a pentamer
D) Three GluN1 subunits and two GluN2 subunits, arranged as a pentamer
E) Two GluN1 subunits and two GluN2 subunits, arranged as a tetramer
Question
What are the three types of ionotropic glutamate receptors?

A) Nicotinic, muscarinic, and kainate
B) Kainate, AMPA, and nicotinic
C) AMPA, NMDA, and nicotinic
D) Kainate, AMPA, and NMDA
E) Kainate, NMDA, and nicotinic
Question
The NMDA type of glutamate ionotropic receptor requires two agonists to be bound to activate this receptor. What are these two agonists?

A) Glutamate and acetylcholine
B) Glutamate and Glycine or D-serine
C) Glycine and D-serine
D) Glycine and acetylcholine
E) D-serine and acetylcholine
Question
If you record EPSCs with a patch electrode from an interneuron in the
CA1 region of a rat hippocampal slice preparation and hold the postsynaptic membrane potential at -80 mV, why is the response not sensitive to blockers of NMDA receptors?

A) There are no NMDA receptors at these synapses.
B) At -80 mV, AMPA receptors are blocked by magnesium.
C) At -80 mV, NMDA receptors do not bind glutamate.
D) At -80 mV, NMDA receptors are blocked by magnesium.
E) At -80 mV, NMDA receptors do not bind glycine or D-serine.
Question
Under which of the following conditions would you expect NMDA receptors to contribute to postsynaptic currents in the hippocampus?

A) Following a single presynaptic action potential
B) Following a train of presynaptic action potentials at high frequency
C) At resting membrane potential
D) After hyperpolarization of the postsynaptic membrane
E) When ionotropic GABA receptors are also activated
Question
What is a competitive antagonist?

A) An inhibitor ligand for a receptor that shares its binding site with the natural activating ligand
B) An agonist ligand for a receptor that shares its binding site with the natural activating ligand
C) An inhibitor ligand for a receptor that does not affect the natural activating ligand's ability to bind the receptor
D) An agonist ligand for a receptor that does not affect the natural activating ligand's ability to bind the receptor
E) A receptor ligand that binds to a part of a receptor that is not involved in natural ligand binding
Question
How does the technique called ionophoresis work?

A) Molecules inside a glass pipet can be expelled by pressure.
B) Molecules inside a glass pipet can be expelled by electrical charge.
C) Molecules inside a glass pipet can be expelled by simple diffusion.
D) Molecules inside a glass pipet can be expelled by suction.
E) Molecules inside a glass pipet can be expelled by concentration gradient.
Question
How are acetylcholine receptors distributed along the muscle membrane?

A) They are at a uniform density all along the muscle membrane.
B) They are distributed in a gradual gradient that increases density gradually with distance away from the NMJ.
C) They are distributed in a gradual gradient that decreases density gradually with distance away from the NMJ.
D) They are highly concentrated directly under the presynaptic terminal at the NMJ.
E) There are no acetylcholine receptors on muscle membrane, only on the nerve terminal at the NMJ.
Question
How does acetylcholine binding to nicotinic receptors alter the permeability of the muscle membrane?

A) The permeability of the postsynaptic membrane is increased to sodium, potassium, and calcium, but not to chloride.
B) The permeability of the postsynaptic membrane is increased to sodium, but not to potassium, calcium, and chloride.
C) The permeability of the postsynaptic membrane is increased to sodium, potassium, calcium, and chloride.
D) The permeability of the postsynaptic membrane is increased to potassium, but not to sodium, calcium, and chloride.
E) The permeability of the postsynaptic membrane is increased to calcium but not to sodium, potassium, and chloride.
Question
What is responsible for the time course of decay of the endplate current recorded at the neuromuscular junction?

A) The time that acetylcholine is bound to the acetylcholine receptor.
B) The mean open time of the presynaptic calcium channel that triggers acetylcholine release.
C) The time course of synaptic vesicle endocytosis at the presynaptic nerve terminal.
D) The mean open time of the acetylcholine receptor channel.
E) The mean open time of the postsynaptic voltage-gated sodium channel.
Question
Why do single channel measurements of acetylcholine receptor currents show that all channel openings reach the same amplitude?

A) When the acetylcholine receptor channel is in the open state, the pore conducts the same amount of current due to the permeation properties of that channel.
B) Acetylcholine receptor channels have the same mean open time.
C) Acetylcholine receptors bind two molecules of acetylcholine.
D) Acetylcholine receptor channels have the same probability of opening.
E) Acetylcholine receptor channels have the same desensitization rate.
Question
How many acetylcholine molecules have to bind to the muscle nicotinic acetylcholine receptor to maximally activate this ionotropic receptor channel?

A) 0
B) 1
C) 2
D) 3
E) 4
Question
Which technique can be used to determine the specific conductance changes in the muscle membrane, and their voltage dependence, after acetylcholine binds to nicotinic receptors?

A) Microelectrode recordings
B) Voltage clamp experiments
C) Measurement of the movement of radioactive isotopes across the cell membrane
D) Fluorescence microscopy
E) Gel electrophoresis
Question
What is the reversal potential for a channel?

A) The membrane potential at which the net current flux through a channel is zero, and on either side of which the net current flux moves in opposite directions
B) The membrane potential at which the net current flux through a channel is outward
C) The membrane potential at which the net current flux through a channel is inward
D) The membrane potential of the presynaptic neuron that triggers an action potential
E) The membrane potential of the presynaptic neuron that triggers transmitter release
Question
What would happen to the synaptic potential amplitude caused by an ionotropic receptor in a postsynaptic neuron (e.g. glutamate-mediated EPSP) if the input resistance of the postsynaptic membrane was decreased?

A) There would be no change in the synaptic potential amplitude.
B) The synaptic potential would become larger in amplitude.
C) The synaptic potential would become smaller in amplitude.
D) The synaptic potential would be blocked.
E) The synaptic potential would reverse in polarity.
Question
At the frog neuromuscular junction, when you block voltage-gated sodium channels selectively in muscle (but not nerve), and then record EPPs (using the microelectrode technique) in response to repeated low frequency nerve stimulation, you see EPPs that are very large (each depolarizes muscle membrane above resting potential to about -30 mV), but these EPPS do not fluctuate significantly when you compare the size of each EPP. Why do these EPPs not vary significantly in amplitude?

A) This very large EPP is above threshold and an action potential is evoked which is all-or-none and thus does not show amplitude fluctuations.
B) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the voltage-gated sodium channel.
C) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the acetylcholine receptor channel.
D) The very large EPP is caused by the release of a fixed large number of transmitter molecules that are not packaged into vesicles.
E) The very large EPP is caused by the release of a fixed number of synaptic vesicles released and this number of vesicles does not change with each stimulation.
Question
The reversal potential for the nicotinic acetylcholine receptor is about -15 mV because it is determined by its selective permeability for

A) sodium ions.
B) potassium ions.
C) sodium and potassium ions.
D) sodium, calcium, and potassium ions.
E) calcium ions.
Question
Which two synaptic specializations are present at neuromuscular synapses, but not at CNS synapses?

A) Postjunctional folds and Schwann cells
B) Synaptic vesicles and active zones
C) Glial cell wrapping and mitochondria
D) Postjunctional folds and mitochondria
E) Postjunctional folds and active zones
Question
What is the principal excitatory transmitter in the CNS?

A) Acetylcholine
B) Glutamate
C) GABA
D) Glycine
E) D-serine
Question
What happens to the reversal potential for IPSPs when chloride is injected into an adult neuron to increase the cytoplasmic concentration of chloride?

A) The reversal potential does not change.
B) The reversal potential becomes more positive.
C) The reversal potential becomes more negative.
D) The reversal potential is zero millivolts.
E) The reversal potential is not affected by the chloride concentration in the cytoplasm.
Question
What is the reversal potential for an IPSP in an adult neuron?

A) Near the threshold for firing an action potential
B) Near the voltage that action potentials reach at their peak
C) Near the neuron resting potential
D) Near zero millivolts
E) IPSPs do not have a reversal potential.
Question
In embryonic neurons, activation of ionotropic GABA or glycine receptors results in

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to hyperpolarization.
C) inward movement of chloride, which leads to depolarization.
D) outward movement of chloride, which leads to depolarization.
E) no net movement of chloride, which does not change membrane potential.
Question
If one impales a neuron with two different intracellular microelectrodes, one to measure membrane potential and a second to pass brief hyperpolarizing current pulses into the cell, why does the size of the measured changes in membrane potential caused by the current pulses decrease when transmitter binds to an ionotropic receptor?

A) The ionotropic receptor inhibits a voltage-gated sodium channel.
B) The ionotropic receptor inhibits a voltage-gated potassium channel.
C) The input resistance of the cell does not change when ionotropic receptor channels open.
D) The input resistance of the cell decreases when ionotropic receptor channels open.
E) The input resistance of the cell increases when ionotropic receptor channels open.
Question
In adult neurons, activation of ionotropic GABA or glycine receptors results in

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to hyperpolarization.
C) inward movement of chloride, which leads to depolarization.
D) outward movement of chloride, which leads to depolarization.
E) no net movement of chloride, which does not change membrane potential.
Question
Presynaptic inhibition is caused by

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to depolarization.
C) an increase in the amount of transmitter released from excitatory nerve terminals.
D) a reduction in the amount of transmitter released from excitatory nerve terminals.
E) both an inward movement of chloride, which leads to hyperpolarization and a reduction in the amount of transmitter released from excitatory nerve terminals.
Question
When electrical synapses are said to be "rectifying," it means they

A) do not conduct ions in either direction.
B) conduct ions equally well in both directions.
C) conduct ions more strongly in one direction than the other.
D) cause only excitation.
E) cause only inhibition.
Question
What does an electrical coupling ratio of 1:6 mean?

A) The presynaptic and postsynaptic cells are not electrically coupled.
B) One out of six cells are electrically coupled.
C) One out of six cells are not electrically coupled.
D) One-Sixth of the postsynaptic voltage change appears in the presynaptic cell.
E) One-Sixth of the presynaptic voltage change appears in the postsynaptic cell.
Question
In the late 1800s, explain why the hypothesis that neurons in the brain communicated with one another by chemical transmitter release was not generally accepted.
Question
If two postsynaptic neurons both receive the same synaptic current, but neuron 1 has a much lower resting conductance than neuron 2, which neuron will experience a larger change in membrane potential cause by the synaptic current, and why?
Question
Explain the voltage-sensitivity of the NMDA type of ionotropic glutamate receptors.
Question
Explain how changes in the developmental expression of different chloride transporters alters the synaptic potential caused by ligand-gated chloride channels that are activated by GABA or Glycine.
Question
Describe the mechanism by which auto-inhibition alters synapse function.
Question
Describe the different functions for presynaptic vs. postsynaptic inhibition.
Question
Explain the mechanisms that are used to concentrate acetylcholine receptors on the postsynaptic membrane of motor endplates.
Question
NMDA and AMPA subtypes of glutamate receptors are differentially regulated during synaptic plasticity, with AMPA receptors moving into or out of the postsynaptic density to alter the strength of chemical transmission. Explain how these two types of receptors are localized to postsynaptic sites of transmitter release and how these localization mechanisms might explain these differences in receptor movement.
Question
When electrical synapses are found in the adult CNS, what have they been shown to useful for?
Question
How does Dopamine modulate electrical coupling in the retina?
Question
How are electrical synapses important creating synchronized oscillations of activity within the cortex?
Question
Why is electrical transmission faster than chemical transmission?
Question
What determines the coupling ratio between electrically couple neurons?
Question
Discuss how the presence of both electrical and chemical synaptic transmission can influence one another.
Question
When electrical synapses are found in the adult CNS, what have they been shown to useful for?
Question
What are the advantages of electrical transmission?
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Deck 11: Mechanisms of Direct Synaptic Transmission
1
How does information transfer occur at electrical synapses?

A) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through connexons (or gap junctions).
B) Electrical depolarization of the nerve terminal causes presynaptic calcium channels to open, leading to the direct excitation of the postsynaptic cell.
C) Electrical depolarization of the nerve terminal causes the release of chemicals that open postsynaptic ligand-gated ion channels which pass current, depolarizing the postsynaptic cell.
D) Electrical depolarization of the nerve terminal directly opens postsynaptic ligand-gated ion channels, which pass current, depolarizing the postsynaptic cell.
E) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through voltage-gated ion channels.
A
2
How does information transfer occur at chemical synapses?

A) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through connexons (or gap junctions).
B) Electrical depolarization of the nerve terminal causes presynaptic calcium channels to open, leading to the direct excitation of the postsynaptic cell.
C) Electrical depolarization of the nerve terminal causes the release of chemicals that open postsynaptic ligand-gated ion channels which pass current, depolarizing the postsynaptic cell.
D) Electrical depolarization of the nerve terminal directly opens postsynaptic ligand-gated ion channels, which pass current, depolarizing the postsynaptic cell.
E) Electrical depolarization of the nerve terminal leads to current flow directly from the presynaptic cell to the postsynaptic cell through voltage-gated ion channels.
C
3
Following years of debate about chemical vs. electrical transmission at synapses in the brain, which form of transmission was found to exist?

A) All neurons in the brain were found to use electrical transmission.
B) All neurons in the brain were found to use chemical transmission.
C) Some neurons in the brain were found to use electrical transmission, others chemical transmission, and some both forms of transmission.
D) All neurons in the brain were found to initially use chemical transmission, and then convert to electrical transmission.
E) All neurons in the brain were found to initially use electrical transmission, and then convert to chemical transmission.
C
4
Dendritic spines are commonly a site for

A) both excitatory and inhibitory synaptic transmission.
B) inhibitory synaptic transmission.
C) excitatory synaptic transmission.
D) storage of transmitter molecules.
E) active zones.
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5
Which of the following does not exist at a direct chemical synapse?

A) Synaptic vesicles
B) 30 nm synaptic cleft
C) Postsynaptic ligand gated ion channel receptors
D) Connexon proteins (gap junctions)
E) Active zones
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6
What is the "synaptic cleft"?

A) The nerve terminal
B) The postsynaptic collection of receptors
C) The space between the presynaptic neuron and the postsynaptic cell
D) The postsynaptic change in membrane potential
E) The active zone
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7
At the NMJ, postjunctional folds radiate into the muscle fiber from the cleft at
Regular intervals. What is their role at neuromuscular synapses?

A) Binding transmitter molecules
B) Increasing the postsynaptic surface area for receptors
C) Reducing the space between the presynaptic and postsynaptic cells
D) Increasing the space between presynaptic and postsynaptic cells
E) Degrading transmitter after binding to receptors
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8
How does acetycholinesterase function at synapses that release acetylcholine?

A) It is a postsynaptic muscarinic receptor blocker.
B) It is a postsynaptic nicotinic receptor blocker.
C) It is a synaptic cleft enzyme that breaks down acetylcholine receptor proteins.
D) It is a presynaptic calcium channel agonist.
E) It is a synaptic cleft enzyme that breaks down the transmitter acetylcholine.
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9
How do transmitters act on the postsynaptic cell at direct chemical synapses?

A) They diffuse across postsynaptic membranes to excite postsynaptic cells.
B) They bind to voltage-gated ion channels to induce postsynaptic current flux.
C) They bind to metabotropic receptors to induce postsynaptic biochemical changes.
D) They bind to ligand-gated ion channels to induce postsynaptic current flux.
E) They bind to extracellular matrix molecules to excite postsynaptic cells.
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10
Synaptic vesicles are concentrated in large numbers within nerve terminals. What is their function?

A) They have no known function.
B) They engulf foreign proteins for degradation.
C) They fuse with mitochondria to transport ATP.
D) They store and deliver active zone proteins to the plasma membrane.
E) They store and release chemical transmitter molecules.
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11
What is an endplate potential?

A) The membrane potential that a nerve terminal will release transmitter.
B) The membrane potential that a postsynaptic muscle cell will reach threshold.
C) Depolarization of the endplate region of the muscle fiber following acetylcholine binding to postsynaptic nicotinic acetylcholine receptors.
D) Hyperpolarization of the endplate region of the muscle fiber following acetylcholine binding to postsynaptic nicotinic acetylcholine receptors.
E) Depolarization of the endplate region of the muscle fiber following acetylcholine binding to muscarinic receptors.
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12
How does the size and shape of the endplate potential change when recorded at different distances from the endplate at the NMJ?

A) The EPP does not change when recorded at different distances from the NMJ.
B) The EPP has the same amplitude but has a slower time course when recorded at increasing distances from the NMJ.
C) The EPP has reduced amplitude but the same time course when recorded at increasing distances from the NMJ.
D) The EPP has both a reduced amplitude and slower time course when recorded at increasing distances from the NMJ.
E) The EPP has both an increased amplitude and slower time course when recorded at increasing distances from the NMJ.
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13
An inhibitory postsynaptic potential (IPSP) occurs when

A) the ligand-gated ion channels with a reversal potential that is more negative than membrane potential open in the postsynaptic membrane in response to transmitter binding.
B) the ligand-gated ion channels with a reversal potential that is more positive than membrane potential open in the postsynaptic membrane in response to transmitter binding.
C) metabotropic receptors are activated by transmitter binding.
D) voltage-gated ion channels open during an action potential.
E) the ligand-gated ion channels without a reversal potential open in the postsynaptic membrane in response to transmitter binding.
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14
Why does the plant alkaloid nicotine cause skeletal muscle contraction?

A) Nicotine causes presynaptic action potentials.
B) Nicotine blocks postsynaptic nicotinic acetylcholine receptors.
C) Nicotine is an agonist at postsynaptic muscarinic acetylcholine receptors.
D) Nicotine is an agonist at postsynaptic nicotinic acetylcholine receptors.
E) Nicotine increases presynaptic calcium channel function, increasing transmitter release.
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15
How do acetycholinesterase drugs (i.e. physostigmine) alter EPPs?

A) Physostigmine prolongs the time course of EPPs.
B) Physostigmine blocks EPPs.
C) Physostigmine shortens the time course of EPPs.
D) Physostigmine has no effect on EPPs.
E) Physostigmine prevents the transmitter release that causes EPPs.
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16
What determines the decay time for an endplate potential?

A) The time course of acetylcholine release from the nerve terminal
B) The time that acetylcholine is present in the synaptic cleft
C) The time constant of the presynaptic nerve cell membrane
D) The mean open time of the acetylcholine receptor channel
E) The time constant of the muscle fiber membrane
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17
What is the subunit composition of the NMDA receptor?

A) Four GluN1 subunits arranged as a tetramer
B) Four GluN2 subunits arranged as a tetramer
C) Two GluN1 subunits and three GluN2 subunits, arranged as a pentamer
D) Three GluN1 subunits and two GluN2 subunits, arranged as a pentamer
E) Two GluN1 subunits and two GluN2 subunits, arranged as a tetramer
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18
What are the three types of ionotropic glutamate receptors?

A) Nicotinic, muscarinic, and kainate
B) Kainate, AMPA, and nicotinic
C) AMPA, NMDA, and nicotinic
D) Kainate, AMPA, and NMDA
E) Kainate, NMDA, and nicotinic
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19
The NMDA type of glutamate ionotropic receptor requires two agonists to be bound to activate this receptor. What are these two agonists?

A) Glutamate and acetylcholine
B) Glutamate and Glycine or D-serine
C) Glycine and D-serine
D) Glycine and acetylcholine
E) D-serine and acetylcholine
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20
If you record EPSCs with a patch electrode from an interneuron in the
CA1 region of a rat hippocampal slice preparation and hold the postsynaptic membrane potential at -80 mV, why is the response not sensitive to blockers of NMDA receptors?

A) There are no NMDA receptors at these synapses.
B) At -80 mV, AMPA receptors are blocked by magnesium.
C) At -80 mV, NMDA receptors do not bind glutamate.
D) At -80 mV, NMDA receptors are blocked by magnesium.
E) At -80 mV, NMDA receptors do not bind glycine or D-serine.
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21
Under which of the following conditions would you expect NMDA receptors to contribute to postsynaptic currents in the hippocampus?

A) Following a single presynaptic action potential
B) Following a train of presynaptic action potentials at high frequency
C) At resting membrane potential
D) After hyperpolarization of the postsynaptic membrane
E) When ionotropic GABA receptors are also activated
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22
What is a competitive antagonist?

A) An inhibitor ligand for a receptor that shares its binding site with the natural activating ligand
B) An agonist ligand for a receptor that shares its binding site with the natural activating ligand
C) An inhibitor ligand for a receptor that does not affect the natural activating ligand's ability to bind the receptor
D) An agonist ligand for a receptor that does not affect the natural activating ligand's ability to bind the receptor
E) A receptor ligand that binds to a part of a receptor that is not involved in natural ligand binding
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23
How does the technique called ionophoresis work?

A) Molecules inside a glass pipet can be expelled by pressure.
B) Molecules inside a glass pipet can be expelled by electrical charge.
C) Molecules inside a glass pipet can be expelled by simple diffusion.
D) Molecules inside a glass pipet can be expelled by suction.
E) Molecules inside a glass pipet can be expelled by concentration gradient.
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24
How are acetylcholine receptors distributed along the muscle membrane?

A) They are at a uniform density all along the muscle membrane.
B) They are distributed in a gradual gradient that increases density gradually with distance away from the NMJ.
C) They are distributed in a gradual gradient that decreases density gradually with distance away from the NMJ.
D) They are highly concentrated directly under the presynaptic terminal at the NMJ.
E) There are no acetylcholine receptors on muscle membrane, only on the nerve terminal at the NMJ.
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25
How does acetylcholine binding to nicotinic receptors alter the permeability of the muscle membrane?

A) The permeability of the postsynaptic membrane is increased to sodium, potassium, and calcium, but not to chloride.
B) The permeability of the postsynaptic membrane is increased to sodium, but not to potassium, calcium, and chloride.
C) The permeability of the postsynaptic membrane is increased to sodium, potassium, calcium, and chloride.
D) The permeability of the postsynaptic membrane is increased to potassium, but not to sodium, calcium, and chloride.
E) The permeability of the postsynaptic membrane is increased to calcium but not to sodium, potassium, and chloride.
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26
What is responsible for the time course of decay of the endplate current recorded at the neuromuscular junction?

A) The time that acetylcholine is bound to the acetylcholine receptor.
B) The mean open time of the presynaptic calcium channel that triggers acetylcholine release.
C) The time course of synaptic vesicle endocytosis at the presynaptic nerve terminal.
D) The mean open time of the acetylcholine receptor channel.
E) The mean open time of the postsynaptic voltage-gated sodium channel.
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27
Why do single channel measurements of acetylcholine receptor currents show that all channel openings reach the same amplitude?

A) When the acetylcholine receptor channel is in the open state, the pore conducts the same amount of current due to the permeation properties of that channel.
B) Acetylcholine receptor channels have the same mean open time.
C) Acetylcholine receptors bind two molecules of acetylcholine.
D) Acetylcholine receptor channels have the same probability of opening.
E) Acetylcholine receptor channels have the same desensitization rate.
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28
How many acetylcholine molecules have to bind to the muscle nicotinic acetylcholine receptor to maximally activate this ionotropic receptor channel?

A) 0
B) 1
C) 2
D) 3
E) 4
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29
Which technique can be used to determine the specific conductance changes in the muscle membrane, and their voltage dependence, after acetylcholine binds to nicotinic receptors?

A) Microelectrode recordings
B) Voltage clamp experiments
C) Measurement of the movement of radioactive isotopes across the cell membrane
D) Fluorescence microscopy
E) Gel electrophoresis
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30
What is the reversal potential for a channel?

A) The membrane potential at which the net current flux through a channel is zero, and on either side of which the net current flux moves in opposite directions
B) The membrane potential at which the net current flux through a channel is outward
C) The membrane potential at which the net current flux through a channel is inward
D) The membrane potential of the presynaptic neuron that triggers an action potential
E) The membrane potential of the presynaptic neuron that triggers transmitter release
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31
What would happen to the synaptic potential amplitude caused by an ionotropic receptor in a postsynaptic neuron (e.g. glutamate-mediated EPSP) if the input resistance of the postsynaptic membrane was decreased?

A) There would be no change in the synaptic potential amplitude.
B) The synaptic potential would become larger in amplitude.
C) The synaptic potential would become smaller in amplitude.
D) The synaptic potential would be blocked.
E) The synaptic potential would reverse in polarity.
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32
At the frog neuromuscular junction, when you block voltage-gated sodium channels selectively in muscle (but not nerve), and then record EPPs (using the microelectrode technique) in response to repeated low frequency nerve stimulation, you see EPPs that are very large (each depolarizes muscle membrane above resting potential to about -30 mV), but these EPPS do not fluctuate significantly when you compare the size of each EPP. Why do these EPPs not vary significantly in amplitude?

A) This very large EPP is above threshold and an action potential is evoked which is all-or-none and thus does not show amplitude fluctuations.
B) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the voltage-gated sodium channel.
C) This very large EPP depolarizes the cell so much that the peak of the EPP is near the reversal potential for the acetylcholine receptor channel.
D) The very large EPP is caused by the release of a fixed large number of transmitter molecules that are not packaged into vesicles.
E) The very large EPP is caused by the release of a fixed number of synaptic vesicles released and this number of vesicles does not change with each stimulation.
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33
The reversal potential for the nicotinic acetylcholine receptor is about -15 mV because it is determined by its selective permeability for

A) sodium ions.
B) potassium ions.
C) sodium and potassium ions.
D) sodium, calcium, and potassium ions.
E) calcium ions.
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34
Which two synaptic specializations are present at neuromuscular synapses, but not at CNS synapses?

A) Postjunctional folds and Schwann cells
B) Synaptic vesicles and active zones
C) Glial cell wrapping and mitochondria
D) Postjunctional folds and mitochondria
E) Postjunctional folds and active zones
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35
What is the principal excitatory transmitter in the CNS?

A) Acetylcholine
B) Glutamate
C) GABA
D) Glycine
E) D-serine
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36
What happens to the reversal potential for IPSPs when chloride is injected into an adult neuron to increase the cytoplasmic concentration of chloride?

A) The reversal potential does not change.
B) The reversal potential becomes more positive.
C) The reversal potential becomes more negative.
D) The reversal potential is zero millivolts.
E) The reversal potential is not affected by the chloride concentration in the cytoplasm.
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37
What is the reversal potential for an IPSP in an adult neuron?

A) Near the threshold for firing an action potential
B) Near the voltage that action potentials reach at their peak
C) Near the neuron resting potential
D) Near zero millivolts
E) IPSPs do not have a reversal potential.
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38
In embryonic neurons, activation of ionotropic GABA or glycine receptors results in

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to hyperpolarization.
C) inward movement of chloride, which leads to depolarization.
D) outward movement of chloride, which leads to depolarization.
E) no net movement of chloride, which does not change membrane potential.
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39
If one impales a neuron with two different intracellular microelectrodes, one to measure membrane potential and a second to pass brief hyperpolarizing current pulses into the cell, why does the size of the measured changes in membrane potential caused by the current pulses decrease when transmitter binds to an ionotropic receptor?

A) The ionotropic receptor inhibits a voltage-gated sodium channel.
B) The ionotropic receptor inhibits a voltage-gated potassium channel.
C) The input resistance of the cell does not change when ionotropic receptor channels open.
D) The input resistance of the cell decreases when ionotropic receptor channels open.
E) The input resistance of the cell increases when ionotropic receptor channels open.
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40
In adult neurons, activation of ionotropic GABA or glycine receptors results in

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to hyperpolarization.
C) inward movement of chloride, which leads to depolarization.
D) outward movement of chloride, which leads to depolarization.
E) no net movement of chloride, which does not change membrane potential.
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41
Presynaptic inhibition is caused by

A) inward movement of chloride, which leads to hyperpolarization.
B) outward movement of chloride, which leads to depolarization.
C) an increase in the amount of transmitter released from excitatory nerve terminals.
D) a reduction in the amount of transmitter released from excitatory nerve terminals.
E) both an inward movement of chloride, which leads to hyperpolarization and a reduction in the amount of transmitter released from excitatory nerve terminals.
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42
When electrical synapses are said to be "rectifying," it means they

A) do not conduct ions in either direction.
B) conduct ions equally well in both directions.
C) conduct ions more strongly in one direction than the other.
D) cause only excitation.
E) cause only inhibition.
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43
What does an electrical coupling ratio of 1:6 mean?

A) The presynaptic and postsynaptic cells are not electrically coupled.
B) One out of six cells are electrically coupled.
C) One out of six cells are not electrically coupled.
D) One-Sixth of the postsynaptic voltage change appears in the presynaptic cell.
E) One-Sixth of the presynaptic voltage change appears in the postsynaptic cell.
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44
In the late 1800s, explain why the hypothesis that neurons in the brain communicated with one another by chemical transmitter release was not generally accepted.
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45
If two postsynaptic neurons both receive the same synaptic current, but neuron 1 has a much lower resting conductance than neuron 2, which neuron will experience a larger change in membrane potential cause by the synaptic current, and why?
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46
Explain the voltage-sensitivity of the NMDA type of ionotropic glutamate receptors.
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47
Explain how changes in the developmental expression of different chloride transporters alters the synaptic potential caused by ligand-gated chloride channels that are activated by GABA or Glycine.
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48
Describe the mechanism by which auto-inhibition alters synapse function.
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49
Describe the different functions for presynaptic vs. postsynaptic inhibition.
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50
Explain the mechanisms that are used to concentrate acetylcholine receptors on the postsynaptic membrane of motor endplates.
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51
NMDA and AMPA subtypes of glutamate receptors are differentially regulated during synaptic plasticity, with AMPA receptors moving into or out of the postsynaptic density to alter the strength of chemical transmission. Explain how these two types of receptors are localized to postsynaptic sites of transmitter release and how these localization mechanisms might explain these differences in receptor movement.
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52
When electrical synapses are found in the adult CNS, what have they been shown to useful for?
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53
How does Dopamine modulate electrical coupling in the retina?
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54
How are electrical synapses important creating synchronized oscillations of activity within the cortex?
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55
Why is electrical transmission faster than chemical transmission?
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56
What determines the coupling ratio between electrically couple neurons?
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57
Discuss how the presence of both electrical and chemical synaptic transmission can influence one another.
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58
When electrical synapses are found in the adult CNS, what have they been shown to useful for?
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59
What are the advantages of electrical transmission?
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