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Action Potential Quiz Practice Test

Boost learning with engaging practice questions

Difficulty: Moderate
Grade: Grade 12
Study OutcomesCheat Sheet
Colorful paper art depicting a trivia quiz on neural signals and action potential

What is an action potential?
A long-lasting change in ion permeability lasting minutes.
A slow, graded change in membrane potential.
A continuous chemical signal transmitted by neurotransmitters.
A rapid, all-or-none electrical signal that travels along a neuron.
An action potential is a rapid, all-or-none electrical impulse essential for neuronal communication. It involves a quick change in membrane potential from resting to a peak and back.
What is the typical resting membrane potential of a neuron?
Approximately -20 mV.
Approximately 0 mV.
Approximately +30 mV.
Approximately -70 mV.
Neurons usually maintain a resting membrane potential around -70 mV due to ionic gradients established by ion pumps and leak channels. This potential is crucial for the generation of an action potential upon reaching threshold.
During the depolarization phase of an action potential, which ion predominantly enters the neuron?
Chloride (Cl-)
Potassium (K+)
Sodium (Na+)
Calcium (Ca2+)
During depolarization, voltage-gated sodium channels open, allowing sodium ions to rapidly enter the neuron. This influx of Na+ causes the membrane potential to become more positive, initiating the action potential.
What is required for a neuron to generate an action potential?
The cell must undergo permanent depolarization.
The membrane potential must reach a certain threshold.
There must be a continuous release of neurotransmitters.
The membrane potential must become more negative.
An action potential is only initiated when the membrane potential reaches a specific threshold, triggering voltage-gated sodium channels to open. This threshold mechanism ensures that the neuron fires in an all-or-none fashion.
What is the purpose of the refractory period following an action potential?
It increases the frequency of action potentials.
It permanently inhibits neuron activity.
It causes continuous stimulation of the neuron.
It prevents the neuron from immediately firing again, allowing recovery.
The refractory period is a short phase following an action potential during which the neuron is unable to fire again immediately. This recovery period ensures proper timing and prevents back-to-back firing, allowing the neuron to reset its ion gradients.
Which sequence correctly represents the phases of an action potential?
Depolarization â†' Hyperpolarization â†' Resting potential â†' Repolarization
Resting potential â†' Depolarization â†' Repolarization â†' Hyperpolarization â†' Return to resting potential
Hyperpolarization â†' Depolarization â†' Resting potential â†' Repolarization
Repolarization â†' Depolarization â†' Hyperpolarization â†' Resting potential
The typical progression of an action potential begins at the resting potential, moves through depolarization and repolarization, then briefly overshoots into hyperpolarization before returning to the resting state. This ordered sequence reflects the underlying ionic fluxes.
Which voltage-gated ion channel is mainly responsible for repolarization during an action potential?
Chloride channels
Potassium channels
Sodium channels
Calcium channels
Repolarization occurs when potassium channels open allowing K+ to exit the neuron, thus returning the membrane potential toward its resting state. This outflow of potassium is essential for ending the depolarized phase.
What does the all-or-none principle indicate about action potentials?
Action potentials can vary gradually in size.
The amplitude of an action potential increases with stronger stimuli.
Once a threshold is reached, an action potential will occur with a fixed amplitude.
Partial depolarization can trigger a weak action potential.
The all-or-none principle means that if the threshold is reached, the neuron fires an action potential with a full, constant amplitude. There is no such thing as a partial action potential, ensuring reliable signal transmission.
How does myelination affect the conduction of action potentials along an axon?
It decreases conduction speed by raising membrane resistance.
It dampens the amplitude of action potentials.
It increases conduction speed by allowing saltatory conduction.
It prevents the initiation of action potentials entirely.
Myelination insulates the axon, enabling action potentials to jump between nodes of Ranvier in a process known as saltatory conduction. This significantly speeds up transmission compared to continuous conduction along unmyelinated fibers.
What role does the sodium-potassium pump play in neuronal activity?
It directly generates the depolarization phase of the action potential.
It restores and maintains the resting membrane potential by actively transporting ions.
It facilitates the immediate reactivation of sodium channels.
It initiates the action potential by opening voltage-gated channels.
The sodium-potassium pump uses ATP to move sodium out of and potassium into the neuron, which is necessary to re-establish the ion gradients after an action potential. This activity is key in maintaining the resting membrane potential.
Which process best describes saltatory conduction in myelinated neurons?
Action potentials jump from one node of Ranvier to the next.
Ions diffuse slowly along the axonal membrane.
Neurotransmitters are released at intervals, causing jumps.
Electrical signals propagate continuously along the entire axon.
Saltatory conduction is the process where action potentials rapidly jump between the nodes of Ranvier in myelinated axons. This jumping mechanism greatly increases the speed of electrical conduction.
What ionic movement is primarily responsible for the repolarization phase of an action potential?
Influx of calcium ions.
Efflux of potassium ions.
Efflux of chloride ions.
Influx of sodium ions.
During repolarization, potassium ions exit the cell through open potassium channels. This outflow reduces the positive charge inside the neuron, bringing the membrane potential back toward its resting level.
During the refractory period, what primarily prevents the neuron from firing again immediately?
Temporary inactivation of voltage-gated sodium channels.
Continued influx of sodium ions.
Immediate reactivation of potassium channels.
Accumulation of potassium inside the cell.
The refractory period is marked by the inactivation of voltage-gated sodium channels, which prevents the neuron from firing again too quickly. This temporary inactivation ensures that action potentials propagate in one direction and maintains proper timing.
How can graded potentials summate to initiate an action potential?
By inhibiting sodium-potassium pump activity.
By directly opening voltage-gated ion channels.
By hyperpolarizing the neuron and then rebounding.
By bringing the membrane potential to the threshold level through summation.
Graded potentials are small changes in membrane potential that, when occurring together, can raise the membrane potential to the threshold level required for an action potential. This process of summation is essential for neuronal excitability.
What is the effect of pharmacologically blocking voltage-gated sodium channels on action potential propagation?
It enhances the amplitude of the action potential.
It prevents the initiation and propagation of the action potential by inhibiting depolarization.
It solely affects the repolarization phase.
It causes an immediate hyperpolarization of the neuron.
Blocking voltage-gated sodium channels stops the rapid sodium influx required for depolarization. As a result, the initiation and propagation of the action potential is effectively inhibited.
How would an increase in extracellular potassium concentration affect the resting membrane potential?
It would make the resting potential less negative (partial depolarization).
It would make the resting potential more negative (hyperpolarization).
It would lead to an immediate generation of an action potential.
It would have no effect on the resting membrane potential.
An increase in extracellular potassium decreases the concentration gradient for potassium efflux, leading to a less negative resting membrane potential. This partial depolarization can alter neuronal excitability.
Which alteration in ion channel behavior is most likely to result in a prolonged action potential duration?
Increased opening of chloride channels during depolarization.
Enhanced inactivation of sodium channels.
A delay in the opening of potassium channels.
Faster recovery from the refractory period.
If the opening of potassium channels is delayed, repolarization takes longer, thereby prolonging the action potential duration. This alteration in channel kinetics can significantly affect the timing of neuronal signaling.
In demyelinating diseases, what is the primary mechanism leading to decreased conduction velocity?
Loss of myelin disrupts saltatory conduction along axons.
Enhanced efficiency of the sodium-potassium pump.
Overactivation of inhibitory neurotransmitter systems.
An increase in the density of voltage-gated sodium channels.
Myelin is essential for saltatory conduction, which allows action potentials to jump rapidly between nodes of Ranvier. Loss of myelin in demyelinating diseases disrupts this process, leading to slower nerve conduction.
How does the inactivation gate of voltage-gated sodium channels contribute to unidirectional action potential propagation?
It prolongs depolarization across the entire neuron.
It prevents reactivation in the recently depolarized segment, ensuring one-way propagation.
It allows backward propagation of the action potential.
It accelerates the opening of adjacent sodium channels.
The inactivation gate temporarily blocks sodium channels after they open, preventing the recently depolarized region from firing again immediately. This ensures the action potential travels in one direction.
In what way can a persistent sodium current contribute to conditions such as epilepsy?
It can lead to prolonged depolarization and increased neuronal firing.
It induces hyperpolarization that stabilizes the membrane potential.
It enhances potassium outflow, reducing excitability.
It results in rapid inactivation of the neuron, preventing firing.
A persistent sodium current means that sodium channels do not fully inactivate, allowing continued influx of sodium and prolonged depolarization. This can increase the likelihood of repetitive firing, a factor in pathological hyperexcitability such as epilepsy.
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Study Outcomes

  1. Analyze the phases of the action potential and their significance in neural signaling.
  2. Explain the role of ions in generating and propagating neural signals.
  3. Distinguish between resting potential and action potential in neurons.
  4. Evaluate how changes in ion channels influence neural function.
  5. Apply key concepts of action potentials to predict outcomes in neuronal behavior.

Action Potential Quiz Review Cheat Sheet

  1. Understand the Resting Membrane Potential - Neurons keep their interior about - 70 mV relative to the outside, thanks to the sodium‑potassium pump and selective ion channels working in concert. This voltage "pre‑charge" is what lets neurons leap into action the moment they sense a signal. OpenStax: Resting Membrane Potential
  2. OpenStax: Resting Membrane Potential
  3. Learn the Phases of an Action Potential - Watch as depolarization, repolarization, and hyperpolarization each dance with sodium and potassium ions to carry the nerve impulse down the axon. Knowing the sequence helps you predict how neurons reset and fire again. Kenhub: Action Potential Phases
  4. Kenhub: Action Potential Phases
  5. Grasp the All‑or‑None Principle - Either a neuron fires a full‑blown action potential or it doesn't fire at all; there's no half‑way. Once the threshold is breached, you get a uniform spike every time, making neural communication crisp and reliable. Kenhub: All‑or‑None Principle
  6. Kenhub: All‑or‑None Principle
  7. Recognize the Role of Voltage‑Gated Ion Channels - These "gates" swing open or shut when the membrane potential shifts, ushering in sodium or potassium to sculpt each phase of the action potential. They're the gatekeepers that make rapid signaling possible. OpenStax: Voltage‑Gated Ion Channels
  8. OpenStax: Voltage‑Gated Ion Channels
  9. Understand Depolarization - Sodium channels fling themselves open, flooding the neuron with Naâťş and flipping the inside from negative to positive in milliseconds. This explosive shift is the "rising phase" that propels the signal forward. OpenStax: Depolarization
  10. OpenStax: Depolarization
  11. Comprehend Repolarization - Next, potassium channels widen and let Kâťş flow out, swinging the membrane voltage back down toward negative. This "falling phase" resets the neuron so it's ready for the next charge. OpenStax: Repolarization
  12. OpenStax: Repolarization
  13. Learn about the Refractory Periods - Right after firing, neurons enter an absolute refractory period where no new spike is possible, then a relative phase where only a super‑strong stimulus will do. These downtime windows ensure signals move one way only. Kenhub: Refractory Periods
  14. Kenhub: Refractory Periods
  15. Explore Saltatory Conduction - In myelinated fibers, action potentials leapfrog from node to node, boosting speed and energy efficiency. Think of it as a neuron's way of taking the express train instead of the local. Britannica: Saltatory Conduction
  16. Britannica: Saltatory Conduction
  17. Understand Synaptic Transmission - When an action potential hits the synapse, it triggers neurotransmitter release that bridges the gap to the next cell. This chemical handshake is how neurons talk to muscles, glands, and each other. OpenStax: Synaptic Transmission
  18. OpenStax: Synaptic Transmission
  19. Review Factors Affecting Conduction Velocity - Axon diameter and myelination level both turbocharge how fast your signals travel. Bigger, well‑insulated fibers are the highways of the nervous system. Kenhub: Conduction Velocity Factors
  20. Kenhub: Conduction Velocity Factors
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