Psychology Quiz: Neuronal Communication
20 questions · exam conditions
0:00
Neuronal CommunicationQuestion 1 of 20

A single brief stimulus fully exceeds threshold and is then doubled. How does the neuron's action potential change?

Amplitude becomes larger
Duration becomes longer
Amplitude stays the same
More action potentials fire
← Back to quizzes

Psychology Quiz

Psychology Quiz: Neuronal Communication

Practice Neuronal Communication in Psychology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Neuronal Communication, giving you a quick way to practice the rules, question types, and explanations that matter most for Psychology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A single brief stimulus fully exceeds threshold and is then doubled. How does the neuron's action potential change?

  1. Amplitude becomes larger
  2. Duration becomes longer
  3. Amplitude stays the same (correct answer)
  4. More action potentials fire
Explanation: An action potential is all-or-none: once a stimulus passes threshold, the neuron fires with a fixed amplitude regardless of how much stronger the stimulus is. Doubling an already suprathreshold brief stimulus does not make the spike larger or longer. The tempting wrong answer is thinking a stronger stimulus should produce a bigger action potential, but intensity is coded by firing rate, not spike amplitude.

Question 2

A brief electrical stimulus triggers an action potential at the midpoint of a resting axon. What occurs?

  1. Two APs travel to the terminal
  2. APs travel in both directions (correct answer)
  3. Two APs travel toward the soma
  4. No AP forms without a synapse
Explanation: A suprathreshold electrical stimulus at the midpoint depolarizes the membrane past threshold, so an action potential is generated at that spot and spreads to adjacent regions on both sides. Since the axon is uniform and has no one-way gate at the stimulus site, the impulse is not restricted to the terminal direction. The tempting error is assuming action potentials always move only toward the terminal, but that is only true when they start at the soma end.

Question 3

Chemical synaptic transmission takes about 0.5 ms longer than axon conduction. Why?

  1. Diffusion across the cleft (correct answer)
  2. Action potentials are slower
  3. Na+ channels stay inactivated
  4. Transmitter breaks down first
Explanation: At a chemical synapse, neurotransmitter must be released, diffuse across the synaptic cleft, and bind receptors; that diffusion adds the roughly 0.5 ms synaptic delay. Axon conduction is fast, so the error is thinking action potentials are slower. Na+ channel inactivation relates to refractory timing, and transmitter breakdown happens after transmission, not before.

Question 4

After an action potential peaks at +30 mV, what directly restores the resting potential?

  1. Na+ exits first, K+ enters
  2. Ca2+ enters and vesicles fuse
  3. Cl- enters and K+ is pumped
  4. Na+ inactivates and K+ exits (correct answer)
Explanation: At the peak of the action potential, voltage-gated Na+ channels inactivate, stopping Na+ entry, while voltage-gated K+ channels open and K+ flows out. This loss of positive charge makes the membrane potential return to rest. The tempting wrong idea is that Na+ exits and K+ enters, but Na+ enters during depolarization and K+ exits during repolarization.

Question 5

Two weak EPSPs occur at one synapse 2 ms apart. Neither alone reaches threshold. What explains firing?

  1. Spatial summation elsewhere
  2. Temporal summation occurs (correct answer)
  3. They cancel each other out
  4. They activate sodium pumps
Explanation: Two rapid EPSPs at the same synapse combine because their effects overlap in time, pushing the membrane potential to threshold. This is temporal summation. The tempting alternative, spatial summation elsewhere, would involve simultaneous inputs at different synapses, not repeated weak inputs at the same one. The events do not cancel, and sodium pumps are not what triggers firing.

Question 6

Myasthenia gravis is an autoimmune disorder that causes muscle weakness. The underlying pathology involves antibodies that bind to and block nicotinic acetylcholine receptors at the neuromuscular junction. This disease is therefore an example of a disruption of:

  1. presynaptic neurotransmitter synthesis.
  2. postsynaptic signal reception. (correct answer)
  3. neurotransmitter reuptake mechanisms.
  4. action potential propagation via saltatory conduction.
Explanation: The pathology of myasthenia gravis centers on the postsynaptic membrane. The presynaptic neuron correctly synthesizes and releases acetylcholine, and the action potential propagates normally. The problem is that the postsynaptic receptors are blocked or destroyed, impairing the ability of the muscle cell to receive the chemical signal and respond to it, leading to weakness.

Question 7

A certain inhibitory neurotransmitter opens ligand-gated channels that are permeable to chloride ions (Cl-). If the resting membrane potential of the postsynaptic neuron is -65 mV and the equilibrium potential for Cl- is -75 mV, the binding of this neurotransmitter will lead to:

  1. an influx of Cl-, causing an EPSP.
  2. an efflux of Cl-, causing an IPSP.
  3. an influx of Cl-, causing an IPSP. (correct answer)
  4. no net movement of Cl-, having no effect on the membrane potential.
Explanation: An ion moves in the direction that will push the membrane potential toward its own equilibrium potential. Here, the membrane is at -65 mV, and the Cl- equilibrium is at -75 mV. To move the potential from -65 mV towards -75 mV (making it more negative), negatively charged Cl- ions must enter the cell. This influx of negative charge makes the neuron more negative (hyperpolarized), which is an inhibitory postsynaptic potential (IPSP).

Question 8

An action potential propagates unidirectionally from the axon hillock to the axon terminal. The phenomenon most directly responsible for preventing the action potential from traveling backward up the axon is the:

  1. high concentration of voltage-gated sodium channels at the axon hillock.
  2. insulating property of the myelin sheath that covers the axon.
  3. absolute refractory period, during which sodium channels are inactivated. (correct answer)
  4. continuous activity of the sodium-potassium pump along the axon.
Explanation: As an action potential travels along the axon, the patch of membrane immediately behind the wave of depolarization is in its absolute refractory period. During this period, the voltage-gated sodium channels are in an inactivated state and cannot be reopened, regardless of the stimulus. This effectively prevents the depolarization from spreading backward and ensures the action potential propagates in one direction.

Question 9

Researchers observing a particular synapse find that postsynaptic potentials are always integer multiples of a base value (e.g., 0.5 mV, 1.0 mV, 1.5 mV, but never 0.7 mV). This phenomenon, known as quantal release, is direct evidence that:

  1. the postsynaptic receptors are only sensitive to specific concentrations of neurotransmitter.
  2. the action potential arriving at the axon terminal is a graded, not all-or-none, event.
  3. the neuron can only undergo temporal summation, not spatial summation.
  4. neurotransmitter is released in discrete packets of a relatively uniform size. (correct answer)
Explanation: When you encounter questions about synaptic transmission, focus on the physical mechanisms of how neurons communicate. Quantal release is a fundamental principle that reveals the discrete, packet-like nature of neurotransmitter release. The key insight here is in the pattern: postsynaptic potentials occur only in integer multiples of a base value. This stepwise pattern directly demonstrates that neurotransmitter isn't released as a continuous stream, but rather in uniform "packets" called vesicles. Each vesicle contains roughly the same amount of neurotransmitter molecules. When one vesicle releases its contents, you get the base response (0.5 mV). When two vesicles release simultaneously, you get double that (1.0 mV), and so on. This is why you see only whole-number multiples, never fractional values like 0.7 mV. Option A incorrectly suggests the receptors cause this pattern, but receptor sensitivity doesn't explain the discrete stepping. Option B confuses the issue entirely—action potentials remain all-or-none events regardless of what happens at the synapse. Option C misidentifies the phenomenon as related to summation types, when quantal release actually supports both spatial and temporal summation. Option D correctly identifies that neurotransmitter release occurs in discrete, uniform packets (vesicles). Remember this connection: whenever you see "quantal" in neuroscience, think "discrete packets." Questions about synaptic transmission often test whether you understand that communication between neurons involves predictable, measurable units of chemical release, not random or continuous amounts.

Question 10

A novel neurotoxin is discovered that selectively and permanently binds to voltage-gated sodium channels, locking them in their inactivated state. If a neuron is exposed to this toxin after it has just fired a single action potential, what will be the long-term consequence for this neuron's ability to communicate?

  1. The neuron will be unable to repolarize its membrane after a subsequent stimulation.
  2. The neuron will be permanently unable to generate another action potential at the axon hillock. (correct answer)
  3. The neuron will be able to fire action potentials, but they will have a smaller amplitude.
  4. The neuron's resting membrane potential will shift to a significantly more positive value.
Explanation: The ability to generate an action potential depends on the ability of voltage-gated sodium channels to open from a closed state. The inactivated state is a temporary state during the refractory period from which channels must recover before they can open again. If the toxin locks them in this inactivated state, they can never be opened, and thus no action potential can be generated. This is distinct from simply blocking the channels; it traps them in a post-firing state.

Question 11

A postsynaptic neuron has a resting potential of -70 mV and a threshold of excitation of -50 mV. It receives simultaneous input from two presynaptic neurons. Neuron A's input causes a 15 mV hyperpolarizing postsynaptic potential (IPSP). Neuron B's input causes a 30 mV depolarizing postsynaptic potential (EPSP). What is the resulting membrane potential, and will the neuron fire an action potential?

  1. The membrane potential will be -55 mV, and an action potential will not be fired. (correct answer)
  2. The membrane potential will be -85 mV, and an action potential will not be fired.
  3. The membrane potential will be -55 mV, and an action potential will be fired.
  4. The membrane potential will be -25 mV, and an action potential will be fired.
Explanation: This problem requires multi-step reasoning involving spatial summation. First, calculate the net change in potential: the +30 mV EPSP and the -15 mV IPSP sum to a net depolarization of +15 mV. Second, apply this change to the resting potential: -70 mV + 15 mV = -55 mV. Third, compare the result to the threshold: -55 mV is at the threshold but does not exceed it. Conventionally, the potential must exceed the threshold to fire. Thus, the final potential is -55 mV, and no action potential is generated.

Question 12

The all-or-none principle states that an action potential maintains a constant amplitude as it travels down an axon. How, then, does the nervous system encode stimulus intensity, such as the difference between a dim light and a bright light?

  1. By altering the speed of action potential propagation; stronger stimuli cause faster propagation.
  2. By increasing the amplitude of the action potential for stronger stimuli.
  3. By varying the frequency of action potentials generated per unit of time. (correct answer)
  4. By releasing different types of neurotransmitters for stimuli of different intensities.
Explanation: The nervous system uses frequency coding to represent stimulus intensity. While the size (amplitude) of each individual action potential is fixed (all-or-none), a stronger stimulus will cause the neuron to fire action potentials more rapidly or frequently. The brain interprets this higher frequency of firing as a more intense stimulus.

Question 13

The 'decision' for a neuron to fire an action potential is made at the axon hillock, where graded potentials are integrated. The axon hillock serves as this integration point because its membrane has a significantly higher density of which component compared to the dendrites or soma?

  1. Voltage-gated sodium channels (correct answer)
  2. Ligand-gated ion channels
  3. Sodium-potassium pumps
  4. Neurotransmitter reuptake transporters
Explanation: The axon hillock (and the adjacent initial segment of the axon) is the spike initiation zone. Its special status comes from having a much higher concentration of voltage-gated sodium channels than the cell body or dendrites. This high density lowers the threshold for generating an action potential in this region, making it the point where the sum of all incoming EPSPs and IPSPs is most likely to trigger a full, all-or-none action potential.

Question 14

A novel neurotoxin is discovered that selectively and permanently binds to voltage-gated sodium channels, locking them in their inactivated state. If a neuron is exposed to this toxin after it has just fired a single action potential, what will be the long-term consequence for this neuron's ability to communicate?

  1. The neuron will be unable to repolarize its membrane after a subsequent stimulation.
  2. The neuron will be permanently unable to generate another action potential at the axon hillock. (correct answer)
  3. The neuron will be able to fire action potentials, but they will have a smaller amplitude.
  4. The neuron's resting membrane potential will shift to a significantly more positive value.
Explanation: The ability to generate an action potential depends on the ability of voltage-gated sodium channels to open from a closed state. The inactivated state is a temporary state during the refractory period from which channels must recover before they can open again. If the toxin locks them in this inactivated state, they can never be opened, and thus no action potential can be generated. This is distinct from simply blocking the channels; it traps them in a post-firing state.

Question 15

A postsynaptic neuron has a resting potential of -70 mV and a threshold of excitation of -50 mV. It receives simultaneous input from two presynaptic neurons. Neuron A's input causes a 15 mV hyperpolarizing postsynaptic potential (IPSP). Neuron B's input causes a 30 mV depolarizing postsynaptic potential (EPSP). What is the resulting membrane potential, and will the neuron fire an action potential?

  1. The membrane potential will be -55 mV, and an action potential will not be fired. (correct answer)
  2. The membrane potential will be -85 mV, and an action potential will not be fired.
  3. The membrane potential will be -55 mV, and an action potential will be fired.
  4. The membrane potential will be -25 mV, and an action potential will be fired.
Explanation: This problem requires multi-step reasoning involving spatial summation. First, calculate the net change in potential: the +30 mV EPSP and the -15 mV IPSP sum to a net depolarization of +15 mV. Second, apply this change to the resting potential: -70 mV + 15 mV = -55 mV. Third, compare the result to the threshold: -55 mV is at the threshold but does not exceed it. Conventionally, the potential must exceed the threshold to fire. Thus, the final potential is -55 mV, and no action potential is generated.

Question 16

A researcher uses a drug that specifically prevents the action of the enzyme acetylcholinesterase at the neuromuscular junction. What is the most likely immediate effect on the postsynaptic muscle cell when the presynaptic neuron fires?

  1. The muscle cell will fail to depolarize because acetylcholine cannot bind to its receptors.
  2. The muscle cell will experience a prolonged period of depolarization and contraction. (correct answer)
  3. The presynaptic neuron will be unable to release acetylcholine into the synaptic cleft.
  4. The muscle cell will become hyperpolarized, preventing it from contracting.
Explanation: Acetylcholinesterase is the enzyme responsible for breaking down acetylcholine in the synaptic cleft, terminating its signal. Inhibiting this enzyme means that acetylcholine will not be cleared from the synapse efficiently. It will continue to bind to postsynaptic receptors, causing prolonged depolarization of the muscle cell and, consequently, a sustained or spastic contraction.

Question 17

The all-or-none principle states that an action potential maintains a constant amplitude as it travels down an axon. How, then, does the nervous system encode stimulus intensity, such as the difference between a dim light and a bright light?

  1. By altering the speed of action potential propagation; stronger stimuli cause faster propagation.
  2. By increasing the amplitude of the action potential for stronger stimuli.
  3. By varying the frequency of action potentials generated per unit of time. (correct answer)
  4. By releasing different types of neurotransmitters for stimuli of different intensities.
Explanation: The nervous system uses frequency coding to represent stimulus intensity. While the size (amplitude) of each individual action potential is fixed (all-or-none), a stronger stimulus will cause the neuron to fire action potentials more rapidly or frequently. The brain interprets this higher frequency of firing as a more intense stimulus.

Question 18

A certain inhibitory neurotransmitter opens ligand-gated channels that are permeable to chloride ions (Cl-). If the resting membrane potential of the postsynaptic neuron is -65 mV and the equilibrium potential for Cl- is -75 mV, the binding of this neurotransmitter will lead to:

  1. an influx of Cl-, causing an EPSP.
  2. an efflux of Cl-, causing an IPSP.
  3. an influx of Cl-, causing an IPSP. (correct answer)
  4. no net movement of Cl-, having no effect on the membrane potential.
Explanation: An ion moves in the direction that will push the membrane potential toward its own equilibrium potential. Here, the membrane is at -65 mV, and the Cl- equilibrium is at -75 mV. To move the potential from -65 mV towards -75 mV (making it more negative), negatively charged Cl- ions must enter the cell. This influx of negative charge makes the neuron more negative (hyperpolarized), which is an inhibitory postsynaptic potential (IPSP).

Question 19

The 'decision' for a neuron to fire an action potential is made at the axon hillock, where graded potentials are integrated. The axon hillock serves as this integration point because its membrane has a significantly higher density of which component compared to the dendrites or soma?

  1. Voltage-gated sodium channels (correct answer)
  2. Ligand-gated ion channels
  3. Sodium-potassium pumps
  4. Neurotransmitter reuptake transporters
Explanation: The axon hillock (and the adjacent initial segment of the axon) is the spike initiation zone. Its special status comes from having a much higher concentration of voltage-gated sodium channels than the cell body or dendrites. This high density lowers the threshold for generating an action potential in this region, making it the point where the sum of all incoming EPSPs and IPSPs is most likely to trigger a full, all-or-none action potential.

Question 20

Myasthenia gravis is an autoimmune disorder that causes muscle weakness. The underlying pathology involves antibodies that bind to and block nicotinic acetylcholine receptors at the neuromuscular junction. This disease is therefore an example of a disruption of:

  1. presynaptic neurotransmitter synthesis.
  2. postsynaptic signal reception. (correct answer)
  3. neurotransmitter reuptake mechanisms.
  4. action potential propagation via saltatory conduction.
Explanation: The pathology of myasthenia gravis centers on the postsynaptic membrane. The presynaptic neuron correctly synthesizes and releases acetylcholine, and the action potential propagates normally. The problem is that the postsynaptic receptors are blocked or destroyed, impairing the ability of the muscle cell to receive the chemical signal and respond to it, leading to weakness.