Synaptic Transmission Study Question Bank
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- 1.
Sequential excitatory postsynaptic potentials (EPSPs) from a given presynaptic terminal will be most effective at bringing a postsynaptic neuron to threshold when:
- A.
Inhibitory inputs are present on the soma
- B.
EPSPs are arriving very close together in time
- C.
EPSPs are arriving from presynaptic cells that form synapses at a great distance from the axon hillox
- D.
Individual excitatory inputs have a low frequency of activity, enabling the membrane to recover from inactivation between EPSPs
Correct Answer
B. EPSPs are arriving very close together in timeExplanation
When EPSPs (excitatory postsynaptic potentials) arrive very close together in time, it means that the postsynaptic neuron is receiving a high frequency of excitatory inputs. This leads to a phenomenon called temporal summation, where the EPSPs add up and increase in amplitude, making it more likely for the postsynaptic neuron to reach its threshold and generate an action potential. Therefore, when EPSPs are arriving very close together in time, they are most effective at bringing the postsynaptic neuron to threshold.Rate this question:
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- 2.
If an inhibitor of acetylcholinesterase is applied to the neuromuscular junction, the muscle contracts in response to the first action potential in the motor neuron but is refractory to the additional stimuli. What is the basis for the refractoriness of the skeletal muscle action potential?
- A.
Continued binding of ACh to receptors in the motor end-plate causes a sustained increase in K+ conductance and hyperpolarization of Vm relative to resting Vm.
- B.
Continued binding of ACh to receptors in the motor end-plate causes an increase in the steady-state level of inactivation of Na+ channels in the muscle membrane adjacent to the endplate and ACh receptor desensitization at the endplate.
- C.
Failure of acetylcholinesterase to hydrolyze ACh makes it impossible for new molecules of ACh to bind to the receptors on the post-synaptic membrane.
- D.
Failure of acetylcholinesterase to hydrolyze ACh results in depletion of ACh in the pre-junctional axon terminal, so that no ACh is released in response to an action potential in the motor neuron.
Correct Answer
B. Continued binding of ACh to receptors in the motor end-plate causes an increase in the steady-state level of inactivation of Na+ channels in the muscle membrane adjacent to the endplate and ACh receptor desensitization at the endplate.Explanation
The refractoriness of the skeletal muscle action potential is due to the continued binding of ACh to receptors in the motor end-plate, which causes an increase in the steady-state level of inactivation of Na+ channels in the muscle membrane adjacent to the endplate. This means that the Na+ channels become less responsive to further stimuli, leading to a decrease in the excitability of the muscle. Additionally, the continued binding of ACh also results in ACh receptor desensitization at the endplate, further contributing to the refractoriness of the muscle action potential.Rate this question:
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- 3.
During an EPSP, there is an increased permeability to both K+ and Na+. Typically, how would the amplitude of the EPSP compare if there was also an increase in membrane permeability to Cl-?
- A.
The amplitude would increase
- B.
The amplitude would decrease
- C.
The amplitude would remain the same
- D.
The amplitude would become zero, i.e., Vm during the EPSP would equal resting Vm.
Correct Answer
B. The amplitude would decreaseExplanation
During an EPSP, there is an increased permeability to both K+ and Na+. If there is also an increase in membrane permeability to Cl-, it would lead to an influx of Cl- ions into the cell, which would counteract the depolarizing effect of the K+ and Na+ ions. This would result in a decrease in the amplitude of the EPSP.Rate this question:
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- 4.
The influx of Ca2+ into the presynaptic terminal during synaptic transmission is due primarily to what?
- A.
A neurotransmitter-mediated increase in membrane gCa
- B.
Depolarization of membrane potential that increases the driving force for inward Ca2+ current (assume ECa = +100 mV)
- C.
A voltage-activated increase in membrane gCa
- D.
Exocytosis
Correct Answer
C. A voltage-activated increase in membrane gCaExplanation
During synaptic transmission, the influx of Ca2+ into the presynaptic terminal is primarily due to a voltage-activated increase in membrane gCa. This means that when the membrane potential of the presynaptic terminal depolarizes, it causes an increase in the conductance of Ca2+ channels in the membrane. This allows Ca2+ ions to flow into the terminal, triggering the release of neurotransmitters from synaptic vesicles through exocytosis. Therefore, the voltage-activated increase in membrane gCa is the main mechanism responsible for the influx of Ca2+ during synaptic transmission.Rate this question:
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- 5.
Of the following, which describes a feature common to synaptic transmission in the CNS and at the neuromuscular junction?
- A.
An action potential in a presynaptic neuron or a motor neuron will trigger an action potential with high likelihood in the postsynaptic neuron or muscle fiber, respectively.
- B.
A single quantum (single vesicle release) of neurotransmitter produces an EPSP or EPP (endplate potential)
- C.
Synaptic transmission in both cases can be modulated by presynaptic inhibition
- D.
The EPSP and EPP are both depolarizing due to an influx of Na+ ions.
Correct Answer
D. The EPSP and EPP are both depolarizing due to an influx of Na+ ions.Explanation
Both the EPSP (excitatory postsynaptic potential) and EPP (endplate potential) are depolarizing because they result from an influx of Na+ ions. This depolarization allows for the propagation of an action potential in the postsynaptic neuron or muscle fiber, respectively. This feature is common to both synaptic transmission in the CNS and at the neuromuscular junction.Rate this question:
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- 6.
Nicotinic ACh receptors are responsible for which of the following events?
- A.
Producing the skeletal muscle end-plate potential
- B.
Decreasing the rate of phase-4 depolarization at the SA node
- C.
Increasing the force of stomach contractions
- D.
Delaying the emptying of liquids from the stomach
- E.
Decreasing the excitability of sympathetic postganglionic neurons
Correct Answer
A. Producing the skeletal muscle end-plate potentialExplanation
Nicotinic ACh receptors are responsible for producing the skeletal muscle end-plate potential. These receptors are located at the neuromuscular junction, where they bind acetylcholine released from motor neurons. This binding triggers the opening of ion channels, allowing the influx of sodium ions into the muscle cell. This influx of sodium ions leads to depolarization of the muscle cell membrane, ultimately causing muscle contraction. Therefore, the activation of nicotinic ACh receptors is crucial for the generation of the end-plate potential and subsequent muscle contraction.Rate this question:
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- 7.
Which of the following statements about synaptic transmission at the neuromuscular junction is true?
- A.
It is enhanced by high levels of cholinesterase
- B.
It is caused by an influx of potassium ions through the muscle membrane
- C.
It is depressed by increased parasympathetic nerve activity
- D.
It is produced by the release of acetylcholine from the alpha motorneuron
Correct Answer
D. It is produced by the release of acetylcholine from the alpHa motorneuronExplanation
Synaptic transmission at the neuromuscular junction is true because it is produced by the release of acetylcholine from the alpha motorneuron. Acetylcholine is a neurotransmitter that is released from the alpha motorneuron and binds to receptors on the muscle membrane, causing muscle contraction. This is the process by which nerve impulses are transmitted from the nervous system to the muscles, allowing for movement and muscle control.Rate this question:
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- 8.
Periodic hyperkalemic paralysis is characterized by high potassium concentration and muscle weakness. Which of the following is likely to cause muscle weakness as a result of increased extracellular potassium concentration?
- A.
Hyperpolarization of muscle cells
- B.
Inactivation of sodium channels in muscle cells
- C.
Increased release of neurotransmitters from alpha motorneurons
- D.
Decreased potassium conductance in muscle cells
- E.
Increased duration of action potentials produced by alpha motorneurons
Correct Answer
B. Inactivation of sodium channels in muscle cellsExplanation
Inactivation of sodium channels in muscle cells is likely to cause muscle weakness as a result of increased extracellular potassium concentration. Sodium channels are responsible for the depolarization phase of action potentials in muscle cells. When these channels are inactivated, it impairs the ability of muscle cells to generate action potentials and contract properly, leading to muscle weakness.Rate this question:
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- 9.
The correct temporal sequence of events at the neuromuscular junction is what?
- A.
. Action potential in the motor nerve; depolarization of the muscle end plate; uptake of Ca2+ into the presynaptic nerve terminal
- B.
Uptake of Ca2+ into the presynaptic terminal; release of acetylcholine (ACh); depolarization of the muscle end plate
- C.
Release of ACh; action potential in the motor nerve; action potential in the muscle
- D.
Uptake of Ca2+ into the motor end plate; action potential in the motor end plate; action potential in the muscle
- E.
Release of ACh; action potential in the muscle end plate; action potential in the muscle
Correct Answer
B. Uptake of Ca2+ into the presynaptic terminal; release of acetylcholine (ACh); depolarization of the muscle end plateExplanation
The correct temporal sequence of events at the neuromuscular junction is as follows: first, there is uptake of Ca2+ into the presynaptic terminal. This is followed by the release of acetylcholine (ACh) into the synaptic cleft. Finally, the muscle end plate depolarizes, leading to muscle contraction.Rate this question:
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- 10.
A person with myasthenia gravis notes increased muscle strength when he is treated with an acetylcholinesterase (AChE) inhibitor. The basis for his improvement is due to the increase in which of the following?
- A.
The amount of acetylcholine (ACh) released from motor nerves
- B.
The level of ACh at the muscle end plates
- C.
The number of ACh receptors on the motor end plates
- D.
The amount of norepinephrine released from motor nerves
- E.
Synthesis of norepinephrine in motor nerves
Correct Answer
B. The level of ACh at the muscle end platesExplanation
When a person with myasthenia gravis is treated with an acetylcholinesterase (AChE) inhibitor, their muscle strength increases. This is because the AChE inhibitor prevents the breakdown of acetylcholine (ACh) at the muscle end plates, leading to an increase in the level of ACh at the muscle end plates. This allows for more efficient transmission of nerve impulses from the motor nerves to the muscles, resulting in improved muscle strength.Rate this question:
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- 11.
At the muscle end plate, acetylcholine (ACh) causes the opening of which of the following?
- A.
Na+ channels and depolarization toward the Na+ equilibrium potential
- B.
K+ channels and depolarization towards the K+ equilibrium potential
- C.
Ca2+ channels and depolarization towards the Ca2+ equilibrium potential
- D.
Na+ and K+ channels and depolarization to a value halfway between the Na+ and K+ equilibrium potentials
- E.
Na+ and K+ channels and hyperpolarization to a value halfway between the Na+ and K+ equilibrium potentials
Correct Answer
D. Na+ and K+ channels and depolarization to a value halfway between the Na+ and K+ equilibrium potentialsExplanation
At the muscle end plate, acetylcholine (ACh) causes the opening of Na+ and K+ channels. This allows both Na+ and K+ ions to flow across the membrane, resulting in depolarization. The depolarization occurs to a value halfway between the Na+ and K+ equilibrium potentials, which means that the membrane potential becomes less negative. This depolarization is necessary for the generation of an action potential and subsequent muscle contraction.Rate this question:
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- 12.
An inhibitory post-synaptic potential changes the membrane potential in which of the following mechanisms?
- A.
Depolarization of the postsynaptic membrane by opening Na+ channels
- B.
Depolarization the postsynaptic membrane by opening K+ channels
- C.
Hyperpolarization the postsynaptic membrane by opening Ca2+ channels
- D.
Hyperpolarization of the postsynaptic membrane by opening Cl- channels
Correct Answer
D. Hyperpolarization of the postsynaptic membrane by opening Cl- channelsExplanation
An inhibitory post-synaptic potential (IPSP) is a hyperpolarization of the postsynaptic membrane, meaning it increases the membrane potential and makes it more negative. This is achieved by opening Cl- channels, allowing Cl- ions to enter the cell, which leads to an influx of negative charge and hyperpolarization.Rate this question:
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- 13.
Which of the following is an inhibitory neurotransmitter in the central nervous system (CNS)?
- A.
Norepinephrine
- B.
Glutamate
- C.
γ-aminobutyric acid (GABA)
- D.
Serotonin
- E.
Histamine
Correct Answer
C. γ-aminobutyric acid (GABA)Explanation
γ-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system (CNS). It functions to reduce neuronal excitability and inhibit the transmission of signals between nerve cells. This helps to regulate and balance the activity of the CNS. Norepinephrine, glutamate, serotonin, and histamine are all excitatory neurotransmitters that promote neuronal activity and transmission.Rate this question:
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- 14.
Which correctly associates a neurotransmitter with one of its characteristics?
- A.
Dopamine is a catecholamine synthesized from the amino acid tyrosine.
- B.
Glutamate is released by most inhibitory interneurons in the spinal cord.
- C.
Serotonin is an endogenous opioid associated with “runner’s high.”
- D.
GABA is the neurotransmitter that mediates long-term potentiation
- E.
Neuropeptides are synthesized in the axons terminals of the neurons that release them
Correct Answer
A. Dopamine is a catecholamine synthesized from the amino acid tyrosine.Explanation
Dopamine is a catecholamine synthesized from the amino acid tyrosine. This means that dopamine is a type of neurotransmitter that belongs to the catecholamine group and is produced from the amino acid tyrosine. Catecholamines are a class of neurotransmitters that include dopamine, norepinephrine, and epinephrine. This association correctly identifies dopamine as a catecholamine and explains its synthesis process.Rate this question:
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- 15.
The NMDA receptor is activated by what neurotransmitter?
- A.
Glycine
- B.
Acetylcholine
- C.
Substance P
- D.
Histamine
- E.
Glutamate
Correct Answer
E. GlutamateExplanation
The NMDA receptor is a type of receptor in the brain that is activated by the neurotransmitter glutamate. Glutamate is the primary excitatory neurotransmitter in the central nervous system and plays a crucial role in various brain functions, including learning, memory, and synaptic plasticity. When glutamate binds to the NMDA receptor, it allows the influx of calcium ions into the neuron, leading to the activation of various signaling pathways and ultimately influencing neuronal communication and plasticity.Rate this question:
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- 16.
Presynaptic inhibition of the central nervous system affects the firing rate of alpha motorneurons by which of the following mechanisms?
- A.
Increasing the Cl- permeability of the presynaptic nerve ending
- B.
Decreasing the K+ permeability of the alpha motorneuron
- C.
Decreasing the frequency of action potentials by the presynaptic nerve ending
- D.
Hyperpolarizing the membrane potential of the alpha motorneuron
- E.
Increasing the amount of neurotransmitter released by the presynaptic nerve ending
Correct Answer
A. Increasing the Cl- permeability of the presynaptic nerve endingExplanation
Presynaptic inhibition refers to the regulation of neurotransmitter release from the presynaptic nerve ending. By increasing the Cl- permeability of the presynaptic nerve ending, the membrane potential becomes more negative, resulting in hyperpolarization. This hyperpolarization reduces the likelihood of an action potential being generated, thus decreasing the frequency of action potentials by the presynaptic nerve ending. As a result, the firing rate of alpha motorneurons is affected, leading to a decrease in muscle contraction.Rate this question:
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Mar 21, 2023Quiz Edited by
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Oct 27, 2011Quiz Created by
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