IB Biology Quiz: Apply Neural Signalling
19 questions · exam conditions
0:00
Apply Neural SignallingQuestion 1 of 19

Following the repolarization phase of an action potential, the membrane potential often briefly becomes more negative than the resting potential. What is the direct cause of this hyperpolarization, or 'undershoot'?

The sodium-potassium pump working at an accelerated rate to remove excess Na+ from the cell.
The voltage-gated potassium channels being slow to close, allowing continued efflux of K+ ions.
An influx of chloride (Cl-) ions through channels that open in response to repolarization.
The inactivation of both voltage-gated Na+ and K+ channels, allowing the potential to be dominated by intracellular anions.
← Back to quizzes

IB Biology Quiz

IB Biology Quiz: Apply Neural Signalling

Practice Apply Neural Signalling in IB Biology 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 Apply Neural Signalling, giving you a quick way to practice the rules, question types, and explanations that matter most for IB Biology.

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

Following the repolarization phase of an action potential, the membrane potential often briefly becomes more negative than the resting potential. What is the direct cause of this hyperpolarization, or 'undershoot'?

  1. The sodium-potassium pump working at an accelerated rate to remove excess Na+ from the cell.
  2. The voltage-gated potassium channels being slow to close, allowing continued efflux of K+ ions. (correct answer)
  3. An influx of chloride (Cl-) ions through channels that open in response to repolarization.
  4. The inactivation of both voltage-gated Na+ and K+ channels, allowing the potential to be dominated by intracellular anions.
Explanation: The hyperpolarization phase occurs because the voltage-gated K+ channels that opened during repolarization are slower to close than the voltage-gated Na+ channels are to inactivate. This means that for a brief period, the membrane's permeability to K+ is even higher than it is at rest. The continued efflux of positive K+ ions drives the membrane potential closer to the K+ equilibrium potential, which is more negative than the resting potential.

Question 2

Tetrodotoxin (TTX) is a potent neurotoxin found in pufferfish that specifically blocks voltage-gated sodium channels. An experiment is conducted where a neuron is placed in a solution containing a sublethal dose of TTX.

If this neuron is then stimulated with a stimulus that would normally be well above the threshold level, what is the most likely outcome?

  1. The neuron will fail to depolarize, and no action potential will be generated. (correct answer)
  2. An action potential of smaller amplitude will be generated due to fewer available Na+ channels.
  3. The neuron will depolarize normally but will be unable to repolarize.
  4. The neuron will hyperpolarize and become less excitable to further stimulation.
Explanation: Action potentials rely on a rapid influx of Na+ through voltage-gated channels for depolarization. By blocking these channels, TTX prevents this influx. Even with a strong stimulus, the membrane cannot depolarize to initiate an action potential. Choice B is incorrect because action potentials are 'all-or-nothing' events; their amplitude is not graded. Choice C describes the effect of blocking K+ channels. Choice D is incorrect as blocking Na+ influx would prevent depolarization, not cause hyperpolarization.

Question 3

A postsynaptic neuron receives input from two presynaptic neurons, X and Y. Neuron X releases an excitatory neurotransmitter, and neuron Y releases an inhibitory neurotransmitter. The resting potential of the postsynaptic neuron is -70 mV and its threshold is -50 mV.

If a single firing from neuron X causes a 10 mV depolarization (an EPSP) and a single firing from neuron Y causes a 10 mV hyperpolarization (an IPSP), what will happen if both neurons X and Y fire simultaneously?

  1. The postsynaptic neuron will depolarize to -60 mV and fire an action potential.
  2. The postsynaptic neuron will hyperpolarize to -80 mV, moving further from the threshold.
  3. The two potentials will cancel each other out, and the membrane potential will remain at -70 mV. (correct answer)
  4. The postsynaptic neuron will depolarize to -50 mV, exactly reaching the threshold potential.
Explanation: This is an example of spatial summation. The EPSP from neuron X (+10 mV) and the IPSP from neuron Y (-10 mV) arrive at the same time. The algebraic sum of these potentials is 0 mV. Therefore, they cancel each other out, and the postsynaptic membrane potential remains at its resting value of -70 mV, so no action potential is fired. The other options represent incorrect calculations of the net potential change.

Question 4

Ouabain is a chemical that irreversibly inhibits the sodium-potassium (Na+/K+) pump. If a neuron is treated with ouabain, what is the most likely long-term consequence for its membrane potential and ability to signal?

  1. The resting membrane potential will gradually move towards 0 mV as ion gradients for Na+ and K+ dissipate, eventually preventing the generation of action potentials. (correct answer)
  2. The membrane will immediately hyperpolarize because the electrogenic effect of the pump is removed, making the neuron less excitable.
  3. The resting potential will remain stable because it is primarily determined by leak channels, but action potentials will have a longer duration.
  4. The neuron will become hyperexcitable because Na+ ions will accumulate inside the cell, bringing the membrane potential closer to the threshold.
Explanation: The Na+/K+ pump is essential for maintaining the steep concentration gradients of Na+ (high outside) and K+ (high inside) across the membrane. Without the pump, these ions will leak down their concentration gradients, causing the gradients to dissipate. As a result, the resting membrane potential, which depends on these gradients, will slowly decay towards zero. Eventually, the gradients will be too weak to support the ion fluxes needed for an action potential. The neuron will become inexcitable.

Question 5

The absolute refractory period is a brief time following an action potential when a second action potential cannot be initiated, regardless of stimulus strength. What is the primary molecular mechanism responsible for this period?

  1. The voltage-gated K+ channels are slow to close, causing a temporary hyperpolarization of the membrane.
  2. The Na+/K+ pump has not yet restored the original ion concentration gradients across the membrane.
  3. The voltage-gated Na+ channels are in an inactivated state and cannot be opened by depolarization. (correct answer)
  4. The supply of neurotransmitter in the presynaptic terminal has been depleted by the first action potential.
Explanation: During the absolute refractory period, the voltage-gated sodium channels have a component (the inactivation gate) that plugs the channel pore. This gate remains closed until the membrane repolarizes. While in this inactivated state, the channel cannot open again, even if the membrane is depolarized. This is the key reason a new action potential cannot be started. Choice A describes the relative refractory period. Choice B is incorrect as the pump is slow and many action potentials can fire before gradients run down. Choice D relates to synaptic transmission, not the properties of the axon membrane itself.

Question 6

The venom of the funnel-web spider contains a toxin that blocks voltage-gated calcium channels in the presynaptic terminals of neurons. What would be the most direct consequence of this venom on a chemical synapse?

  1. The action potential would fail to propagate along the axon to reach the presynaptic terminal.
  2. The reuptake of neurotransmitters from the synaptic cleft would be inhibited, causing prolonged stimulation.
  3. Neurotransmitters would be released, but they would be unable to bind to postsynaptic receptors.
  4. The presynaptic terminal would be unable to release neurotransmitters into the synaptic cleft. (correct answer)
Explanation: The arrival of an action potential at the presynaptic terminal opens voltage-gated Ca2+ channels. The subsequent influx of Ca2+ is the critical trigger for the fusion of synaptic vesicles with the presynaptic membrane and the release of neurotransmitters. By blocking these Ca2+ channels, the toxin prevents this trigger, thus blocking neurotransmitter release and synaptic transmission. The action potential itself can still reach the terminal (A), and the toxin does not affect reuptake (B) or receptor binding (D).

Question 7

Considering the factors that influence the speed of nerve impulse conduction, which of the following neurons would transmit an action potential the fastest?

  1. A narrow-diameter, unmyelinated axon found in a simple invertebrate.
  2. A wide-diameter, unmyelinated 'giant' axon, such as that found in a squid.
  3. A narrow-diameter, myelinated axon, such as a pain receptor in a mammal.
  4. A wide-diameter, myelinated axon, such as a motor neuron in a mammal. (correct answer)
Explanation: Two main factors increase conduction velocity: axon diameter and myelination. A wider diameter reduces the internal resistance to the flow of local currents. Myelination allows for saltatory conduction, where the action potential jumps between nodes of Ranvier. A neuron that has both a wide diameter and is myelinated will have the fastest possible conduction speed. The other options are missing one or both of these features.

Question 8

Action potentials are 'all-or-nothing' events of a fixed amplitude. How, then, does the nervous system encode information about the intensity of a stimulus, such as distinguishing a dim light from a bright light?

  1. By increasing the amplitude of individual action potentials for stronger stimuli.
  2. By increasing the speed at which action potentials travel along the axon for stronger stimuli.
  3. By recruiting different types of neurons that fire action potentials of varying sizes.
  4. By increasing the frequency of action potentials fired per unit of time for stronger stimuli. (correct answer)
Explanation: The nervous system uses frequency modulation to encode stimulus intensity. A stronger stimulus (like a bright light) will cause a sensory neuron to fire action potentials at a higher rate (more potentials per second) than a weaker stimulus (a dim light). The amplitude and speed of each individual action potential remain constant for a given neuron. This change in frequency is interpreted by the central nervous system as a change in stimulus intensity.

Question 9

The resting potential of a neuron (around -70 mV) is primarily established by the differential permeability of the membrane to certain ions. Which statement most accurately describes this situation? (HL Content)

  1. The membrane is slightly permeable to Na+ and highly permeable to K+, allowing K+ to leak out down its concentration gradient, making the inside negative. (correct answer)
  2. The membrane is impermeable to all ions, and the negative potential is created solely by the Na+/K+ pump pushing more positive charge out than in.
  3. The membrane is highly permeable to Na+ and slightly permeable to K+, allowing Na+ to leak in and create a steep potential.
  4. The membrane is equally permeable to Na+ and K+, but the Na+/K+ pump activity results in a net negative charge inside the cell.
Explanation: The resting potential is primarily due to potassium leak channels, which make the membrane much more permeable to K+ than to other ions like Na+. Since the concentration of K+ is high inside the cell, K+ ions diffuse out down their concentration gradient, taking positive charge with them. This leaves the inside of the cell with a net negative charge. The Na+/K+ pump maintains these gradients but the potential itself is set by the K+ diffusion through leak channels. Choice C would result in a positive resting potential. Choices B and D misrepresent the role of permeability.

Question 10

In a simple reflex arc, such as withdrawing a hand from a hot object, a sensory neuron synapses directly with a motor neuron in the spinal cord, which then causes a muscle to contract.

In many real reflex arcs, a relay neuron (interneuron) is located between the sensory and motor neuron. What is a primary functional advantage of including a relay neuron in the circuit?

  1. It slows down the reflex action to allow for conscious intervention from the brain.
  2. It allows for the integration of signals, such as inhibiting an opposing muscle group during the reflex. (correct answer)
  3. It reverses the direction of the nerve impulse, sending it back to the sensory receptor for feedback.
  4. It converts the electrical signal of the action potential into a chemical signal, which is not possible without it.
Explanation: Relay neurons allow for more complex processing within the spinal cord. A single sensory neuron can synapse with multiple relay neurons. One relay neuron might excite the flexor motor neuron (to pull the hand away), while another, inhibitory, relay neuron synapses with the motor neuron for the opposing extensor muscle, causing it to relax. This coordination of opposing muscles (reciprocal inhibition) makes the reflex more efficient and is a key role of interneurons. A is incorrect as reflexes are fast and subconscious. C is incorrect. D is incorrect as the sensory-motor synapse is also chemical.

Question 11

Curare is a plant-derived toxin that acts as a competitive antagonist at nicotinic acetylcholine receptors on the motor end plate of skeletal muscle cells. What is the direct physiological effect of curare poisoning?

  1. It causes continuous, spastic muscle contraction by mimicking the action of acetylcholine.
  2. It prevents the release of acetylcholine from the presynaptic motor neuron terminal.
  3. It inhibits the enzyme acetylcholinesterase, leading to an accumulation of acetylcholine in the synapse.
  4. It blocks the action of acetylcholine, preventing depolarization of the muscle fiber and causing flaccid paralysis. (correct answer)
Explanation: As a competitive antagonist, curare binds to the acetylcholine receptors without activating them. This physically blocks acetylcholine from binding. Without acetylcholine binding, the ligand-gated ion channels on the muscle cell membrane do not open, preventing depolarization and subsequent muscle contraction. This results in muscle weakness and flaccid paralysis. Choice A describes an agonist. Choices B and D describe toxins that act on the presynaptic terminal or on enzymes in the cleft, respectively, not the postsynaptic receptor.

Question 12

Multiple sclerosis is an autoimmune disease where the body's immune system progressively destroys the myelin sheath of neurons in the central nervous system.

Which of the following best explains why this demyelination impairs nerve impulse transmission, leading to symptoms like muscle weakness and poor coordination?

  1. The absence of myelin allows local currents to dissipate, preventing the membrane at the next node of Ranvier from reaching threshold potential. (correct answer)
  2. The destruction of myelin blocks the reuptake of neurotransmitters at the synapse, causing continuous, uncoordinated muscle firing.
  3. Demyelination causes the resting membrane potential to become hyperpolarized, making it much more difficult to initiate any action potential.
  4. The speed of diffusion of neurotransmitters across the synaptic cleft is significantly reduced without the insulation provided by myelin.
Explanation: Myelin acts as an electrical insulator, preventing ion leakage across the axon membrane. This allows the local current generated during an action potential to travel further and faster to the next node of Ranvier, triggering depolarization there. Without myelin, this current dissipates, and the signal may not be strong enough to reach threshold at the next node, effectively blocking propagation. The other options describe effects on the synapse (B, D) or resting potential (C) that are not the primary consequence of demyelination.

Question 13

A researcher is studying a synapse where the neurotransmitter GABA (gamma-aminobutyric acid) is released. GABA is the primary inhibitory neurotransmitter in the central nervous system.

How does the binding of GABA to a postsynaptic GABAA receptor typically prevent the postsynaptic neuron from firing an action potential? (HL Content)

  1. It opens ligand-gated Na+ channels, causing a strong excitatory postsynaptic potential (EPSP).
  2. It opens ligand-gated Cl- channels, causing an influx of negative ions and hyperpolarization (an IPSP). (correct answer)
  3. It blocks voltage-gated K+ channels, preventing the repolarization phase of any potential action potential.
  4. It triggers the release of calcium from internal stores, causing a long-term change in gene expression.
Explanation: GABAA receptors are ligand-gated chloride ion channels. When GABA binds, the channel opens, allowing negatively charged chloride ions (Cl-) to flow into the cell. This influx of negative charge makes the inside of the membrane more negative, a process called hyperpolarization. This creates an inhibitory postsynaptic potential (IPSP), which moves the membrane potential further away from the threshold, making it less likely to fire an action potential. The other options describe excitatory or unrelated mechanisms.

Question 14

A class of antidepressant drugs known as Selective Serotonin Reuptake Inhibitors (SSRIs) functions by blocking the serotonin transporter protein on the presynaptic membrane.

What is the direct effect of an SSRI that leads to its therapeutic action?

  1. It increases the amount of serotonin synthesized and stored in vesicles within the presynaptic neuron.
  2. It acts as an agonist by binding to and activating postsynaptic serotonin receptors, mimicking serotonin.
  3. It prolongs the presence of serotonin in the synaptic cleft, increasing the likelihood of binding to postsynaptic receptors. (correct answer)
  4. It directly increases the number and sensitivity of serotonin receptors on the postsynaptic membrane.
Explanation: Reuptake is the process by which neurotransmitters are cleared from the synaptic cleft back into the presynaptic neuron. By inhibiting the serotonin transporter, SSRIs block this reuptake. This causes serotonin to remain in the synapse for a longer period, allowing it to repeatedly stimulate the postsynaptic receptors. This enhanced stimulation is believed to be the basis of its therapeutic effect. The other options describe different pharmacological mechanisms.

Question 15

Which structural feature of a chemical synapse is most directly responsible for ensuring that nerve impulses are transmitted in only one direction, from the presynaptic to the postsynaptic neuron?

  1. The unidirectional flow of ions through voltage-gated channels along the axon.
  2. The presence of the myelin sheath, which directs the flow of the electrical signal.
  3. The location of synaptic vesicles in the presynaptic terminal and receptors on the postsynaptic membrane. (correct answer)
  4. The action of the refractory period, which prevents the action potential from traveling backward across the synapse.
Explanation: Unidirectional flow is guaranteed by the physical separation of the signal-releasing machinery and the signal-receiving machinery. Neurotransmitters are stored in vesicles and released from the presynaptic terminal. The specific protein receptors that bind these neurotransmitters are embedded in the membrane of the postsynaptic neuron. There are no vesicles on the postsynaptic side and no receptors on the presynaptic side, so the signal can only travel in one direction across the cleft. The refractory period (D) ensures unidirectional flow along an axon, not across a synapse.

Question 16

A local anesthetic such as lidocaine works by blocking voltage-gated sodium channels. Why does this action prevent the sensation of pain?

  1. It prevents sensory neurons from generating and propagating action potentials to the central nervous system. (correct answer)
  2. It hyperpolarizes the neuron's membrane, making it impossible to reach the threshold potential.
  3. It blocks the release of neurotransmitters at the synapse between the sensory neuron and the spinal cord neuron.
  4. It directly binds to pain receptors in the skin, preventing them from detecting the stimulus in the first place.
Explanation: The sensation of pain is transmitted to the brain via action potentials in sensory neurons. Lidocaine blocks the voltage-gated sodium channels that are essential for the depolarization phase of an action potential. Without functioning sodium channels, the neuron cannot fire an action potential, even if it is stimulated by a painful event. Therefore, the pain signal is never generated or propagated to the brain. While it does prevent neurotransmitter release (C), this is a downstream consequence of blocking the action potential itself (A), which is the primary mechanism.

Question 17

A patient suffers an injury that severs the ventral root of a spinal nerve in their lumbar region. Which of the following symptoms would be the most direct result of this specific injury?

  1. Loss of sensation in the corresponding area of the leg, but with retained muscle control.
  2. Loss of both sensation and voluntary muscle control in the corresponding area of the arm.
  3. Loss of voluntary muscle control in the corresponding area of the leg, but with retained sensation. (correct answer)
  4. An inability to process reflex actions in the leg, but with normal voluntary movement and sensation.
Explanation: The ventral root of a spinal nerve contains the axons of motor neurons, which carry signals from the spinal cord to the muscles. Severing this root would interrupt motor commands, causing paralysis in the corresponding area. The dorsal root, which carries sensory information, would be unaffected, so sensation would be retained. Choice A describes damage to a dorsal root. Choice B is incorrect because the injury is in the lumbar (leg) region, not the cervical (arm) region. Choice D is incorrect because both reflex and voluntary motor commands would be blocked.

Question 18

An action potential propagates along an axon as a wave of depolarization. What is the immediate cause of the depolarization of the membrane segment just ahead of the advancing action potential?

  1. The release of neurotransmitters from the preceding segment of the axon that diffuse forward.
  2. The active transport of Na+ ions into the cell by the Na+/K+ pump in the adjacent membrane segment.
  3. The diffusion of Na+ ions along the inside of the axon from the adjacent depolarized region, creating a local current. (correct answer)
  4. The opening of voltage-gated K+ channels in the adjacent membrane segment, initiated by the previous segment.
Explanation: When one segment of the axon depolarizes due to Na+ influx, these positive ions diffuse laterally inside the axon. This movement of charge, known as a local current, depolarizes the adjacent segment of the membrane to its threshold potential. This triggers the opening of voltage-gated Na+ channels in that new segment, continuing the propagation of the action potential. Neurotransmitters are at synapses (A), the pump works against this process (B), and K+ channel opening causes repolarization (D).

Question 19

During the repolarization phase of an action potential, what is the state of the primary voltage-gated ion channels involved in generating the potential?

  1. Voltage-gated Na+ channels are open, while voltage-gated K+ channels are closed.
  2. Voltage-gated Na+ channels are inactivated, while voltage-gated K+ channels are open. (correct answer)
  3. Both voltage-gated Na+ and K+ channels are closed, returning the membrane to resting potential.
  4. Both voltage-gated Na+ and K+ channels are open, leading to a rapid change in membrane potential.
Explanation: Repolarization is caused by the closing and inactivation of voltage-gated Na+ channels and the opening of voltage-gated K+ channels. The efflux of K+ ions out of the cell makes the membrane potential negative again. Choice A describes depolarization. Choice C is incorrect because K+ channels are open. Choice D is incorrect because Na+ channels are inactivated, not open, during repolarization.