Action Potential Generation and Propagation — MCQs

10 questions

Which of the following is/are true about nodes of Ranvier? 1. No myelin 2. Rich in sodium channels

Sequence the events in neuromuscular action potential conduction: 1. Sodium channels open in the end plate 2. Calcium enters at the nerve terminal 3. Release of acetylcholine

How many phases are there in the action potential of cardiac muscles?

Duration of maximum contraction depends upon?

Which of the following statements about the Na-K pump is false?

A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.

Which of the following is true regarding Na+ (sodium) ions?

A patient exhibits hyperkalemia. Which of the following explains how this condition affects nerve excitability?

Absolute refractoriness of a neuron is due to?

Q10

Which of the following is NOT a characteristic of a biphasic action potential of a mixed nerve?

Action Potential Generation and Propagation Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following is/are true about nodes of Ranvier? 1. No myelin 2. Rich in sodium channels

A. None of the options
B. No myelin
C. Both (Correct Answer)
D. Rich in sodium channels

Explanation: ***Both*** - Nodes of Ranvier are **gaps in the myelin sheath** that occur at regular intervals along a myelinated axon, making them areas with **no myelin**. - These nodes are crucially important because they have a **high concentration of voltage-gated sodium channels**, which enables the propagation of action potentials via **saltatory conduction**. - Both statements are **physiologically accurate** descriptions of the nodes of Ranvier, and their unique structure and composition are fundamental to **efficient transmission of nerve impulses**. *None of the options* - This option is incorrect because both statements, "No myelin" and "Rich in sodium channels," are **physiologically accurate** descriptions of the nodes of Ranvier. *No myelin* - While it is true that nodes of Ranvier are **devoid of myelin**, this statement alone does not encompass the full functional importance of these structures. - Their role in nerve impulse conduction also heavily relies on the presence of specific ion channels, which this option does not include. *Rich in sodium channels* - It is accurate that nodes of Ranvier have a **high density of voltage-gated sodium channels**, which is essential for regenerating the action potential. - However, this statement alone omits the key structural feature that they are also **unmyelinated gaps**, which is equally important to their function.

Question 2: Sequence the events in neuromuscular action potential conduction: 1. Sodium channels open in the end plate 2. Calcium enters at the nerve terminal 3. Release of acetylcholine

A. $1 \rightarrow 2 \rightarrow 3$
B. $1 \rightarrow 3 \rightarrow 2$
C. $3 \rightarrow 2 \rightarrow 1$
D. $2 \rightarrow 3 \rightarrow 1$ (Correct Answer)

Explanation: ***Correct: $2 \rightarrow 3 \rightarrow 1$*** - **Calcium entry at the nerve terminal** is the initial trigger - when an action potential reaches the presynaptic nerve terminal, voltage-gated calcium channels open, allowing Ca²⁺ influx - **Acetylcholine release** follows - the increased intracellular calcium causes synaptic vesicles containing acetylcholine to fuse with the presynaptic membrane and release the neurotransmitter into the synaptic cleft - **Sodium channels open in the end plate** last - acetylcholine binds to nicotinic receptors on the motor end plate, opening ligand-gated sodium channels, which depolarizes the muscle membrane and triggers muscle contraction *Incorrect: $1 \rightarrow 2 \rightarrow 3$* - Places sodium channel opening first, which is physiologically impossible - Sodium channels at the motor end plate only open in response to acetylcholine binding - Cannot occur before acetylcholine is released from the nerve terminal *Incorrect: $1 \rightarrow 3 \rightarrow 2$* - Incorrectly sequences sodium channel opening before calcium entry - Violates the fundamental principle that calcium influx is required for neurotransmitter release - Acetylcholine cannot be released without prior calcium entry *Incorrect: $3 \rightarrow 2 \rightarrow 1$* - Places acetylcholine release before calcium entry, which is impossible - Calcium-triggered exocytosis is an absolute requirement for neurotransmitter release - Without calcium influx, vesicles cannot fuse with the presynaptic membrane

Question 3: How many phases are there in the action potential of cardiac muscles?

A. 2 phases
B. 3 phases
C. 4 phases
D. 5 phases (Correct Answer)

Explanation: ***5 phases*** - The cardiac myocyte action potential is classically described in **five phases** (phases 0, 1, 2, 3, and 4), which encompass depolarization, repolarization, and the resting state. - Each phase is characterized by specific ion channel activities leading to distinct electrical changes essential for proper cardiac function. *2 phases* - Action potentials in nerve cells typically follow a simpler two-phase model: **depolarization** and **repolarization**. - This model does not account for the additional plateau and resting phases characteristic of cardiac muscle cells. *3 phases* - Some simplified models might describe three phases (depolarization, repolarization, and a resting phase), but this still **omits specific nuances** of cardiac repolarization and the sustained plateau phase. - This simplification leaves out the early repolarization and the critical plateau phase (phase 2), which is vital for the prolonged contraction of the heart. *4 phases* - While some sources might refer to four phases, they typically combine certain repolarization steps or omit the distinct early repolarization phase. - This description would likely miss the **early, rapid repolarization phase (phase 1)**, understating the complex ion movements.

Question 4: Duration of maximum contraction depends upon?

A. Both
B. Absolute refractory period (Correct Answer)
C. None of the two
D. Relative refractory period

Explanation: ***Absolute refractory period*** - The duration of **maximum (sustained) contraction** in skeletal muscle depends primarily on the **absolute refractory period** - The absolute refractory period (1-2 ms in skeletal muscle) is much **shorter than the contraction duration** (20-200 ms), allowing for **temporal summation** - When stimuli arrive after the refractory period but before complete relaxation, contractions **summate** to produce **tetanus** (sustained maximum contraction) - A shorter refractory period allows **higher frequency stimulation** → more complete summation → stronger and longer sustained contraction - This is why skeletal muscle can achieve **complete tetanus** at stimulation frequencies of 50-100 Hz *Relative refractory period* - While the relative refractory period affects excitability, it is the **absolute refractory period** that sets the fundamental limit on maximum stimulation frequency - The relative refractory period is less critical for determining the duration of maximum contraction *None of the two* - This is incorrect because the refractory period directly determines the **maximum frequency** at which muscle can be stimulated - Higher stimulation frequency (limited by refractory period) → better temporal summation → sustained maximum contraction (tetanus) - The refractory period is the key factor enabling or limiting the duration of maximum contraction *Both* - While both refractory periods influence excitability, the **absolute refractory period** is the primary determinant - It sets the absolute limit on stimulation frequency and thus the ability to achieve and maintain tetanic contraction

Question 5: Which of the following statements about the Na-K pump is false?

A. It is not directly involved in the generation of action potentials.
B. It is electrogenic
C. It needs ATP for its functioning
D. It is located on the apical membrane of cell (Correct Answer)

Explanation: ***It is located on the apical membrane of cell*** - The **Na-K pump**, or **Na+/K+-ATPase**, is primarily located on the **basolateral membrane** of epithelial cells, not **apical membrane**. - Its strategic placement on the basolateral membrane is crucial for maintaining cellular polarity and driving transepithelial transport processes, such as reabsorption in the kidneys. *It is electrogenic* - The Na-K pump is indeed **electrogenic** because it transports three **Na+ ions** out of the cell for every two **K+ ions** pumped in. - This unequal charge distribution creates a net movement of one positive charge out of the cell, contributing to the **resting membrane potential**. *It is not directly involved in the generation of action potentials.* - While the Na-K pump is essential for **maintaining the ion gradients** necessary for **action potentials**, it is not directly involved in their rapid depolarization or repolarization phases. - Action potentials are primarily generated by the rapid opening and closing of **voltage-gated ion channels** (e.g., Na+ and K+ channels). *It needs ATP for its functioning* - The Na-K pump is an **active transport mechanism** that moves ions against their concentration gradients, requiring **energy in the form of ATP hydrolysis**. - This **ATP-dependent process** ensures the continuous maintenance of the Na+ and K+ gradients, crucial for various cellular functions, including nerve impulse transmission and muscle contraction.

Question 6: A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.

A. Assertion is false, but Reason is true
B. Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion (Correct Answer)
C. Both Assertion and Reason are true, and Reason is the correct explanation for Assertion
D. Assertion is true, but Reason is false

Explanation: ***Both Assertion and Reason are true, and Reason is NOT the correct explanation for Assertion*** - The **Assertion** is true: Local anesthetics (like lignocaine) block nerve conduction by inhibiting **voltage-gated sodium channels**, preventing the depolarization necessary for action potential propagation - The **Reason** is also true: Small diameter and non-myelinated fibers (like C and Aδ pain fibers) are blocked more easily than large myelinated fibers (like Aα motor fibers), which explains the **differential blockade** pattern seen clinically - However, the **Reason does NOT explain WHY** local anesthetics block nerve conduction—it describes **WHICH** nerve fibers are blocked preferentially. The mechanism of blocking conduction is sodium channel inhibition, not fiber size selectivity - The differential sensitivity is a consequence of fiber characteristics (surface area-to-volume ratio, number of nodes of Ranvier), not the explanation for the blocking mechanism itself *Both Assertion and Reason are true, and Reason is the correct explanation for Assertion* - While both statements are individually true, the Reason does not explain the **mechanism** by which local anesthetics block nerve conduction - The Reason addresses fiber **selectivity**, which is a separate pharmacological property from the **mechanism of action** (sodium channel blockade) *Assertion is true, but Reason is false* - The Assertion is demonstrably true—local anesthetics block nerve conduction - The Reason is also true—this is well-established pharmacology: autonomic (small) > sensory (medium) > motor (large) fiber blockade sequence *Assertion is false, but Reason is true* - The Assertion is fundamentally correct and represents the primary pharmacological action of local anesthetics - Blocking nerve conduction is the therapeutic goal of local anesthetic administration

Question 7: Which of the following is true regarding Na+ (sodium) ions?

A. Does not help other ions in transport
B. Responsible for depolarization (Correct Answer)
C. Responsible for the resting membrane potential
D. Sodium ion is responsible for Donnan effect

Explanation: ***Responsible for depolarization*** - The rapid influx of **Na+ ions** into the cell through voltage-gated sodium channels is the primary event that causes **depolarization** during an action potential. - This influx makes the inside of the cell more positive, shifting the membrane potential from negative toward positive values. *Sodium ion is responsible for Donnan effect* - The **Donnan effect** describes the unequal distribution of permeable ions across a semi-permeable membrane due to the presence of impermeant charged molecules (e.g., proteins). - **Na+ ions are small, permeable ions** - they do not create the Donnan effect. The effect is caused by large, non-diffusible charged molecules like proteins, not by sodium ions. *Does not help other ions in transport* - The **sodium-potassium pump (Na+/K+-ATPase)** actively transports Na+ out of the cell and K+ into the cell, maintaining their concentration gradients. - These Na+ gradients are crucial for **secondary active transport**, where the energy from Na+ moving down its electrochemical gradient is used to move other ions (e.g., in Na+-glucose cotransport) or molecules against their gradients. *Responsible for the resting membrane potential* - The **resting membrane potential** is primarily established by the differential permeability of the membrane to K+ ions and the activity of the Na+/K+-ATPase. - While Na+ leaking into the cell contributes slightly, the dominant factor is the efflux of **K+ ions** through leak channels, as the membrane is much more permeable to K+ than to Na+ at rest.

Question 8: A patient exhibits hyperkalemia. Which of the following explains how this condition affects nerve excitability?

A. Increases resting membrane potential (Correct Answer)
B. Increases action potential threshold
C. Decreases action potential threshold
D. Decreases membrane potential

Explanation: ***Increases resting membrane potential (makes it less negative/depolarized)*** - **Hyperkalemia** (elevated extracellular K⁺) **depolarizes the resting membrane potential**, making it **less negative** (e.g., from -70 mV to -60 mV). - This occurs because the **Nernst equilibrium potential for K⁺** becomes less negative when extracellular K⁺ increases, shifting the resting potential closer to 0 mV. - The membrane potential moves **closer to the threshold** (which remains constant at ~-55 mV), **initially increasing excitability**. - However, prolonged depolarization causes **inactivation of voltage-gated Na⁺ channels**, leading to **paradoxical decreased excitability**. - Note: The term "increases" here means the membrane potential becomes **less negative** (moves toward 0 mV), not that it becomes more polarized. *Increases action potential threshold* - The **action potential threshold remains constant** at approximately -55 mV and does **not change** with hyperkalemia. - What changes is the **resting membrane potential**, not the threshold. *Decreases action potential threshold* - The **threshold potential does not decrease** in hyperkalemia; it remains fixed at ~-55 mV. - The misconception arises from confusing the **gap between resting potential and threshold** (which decreases) with the **threshold itself** (which stays constant). - While the membrane potential moves closer to threshold, the threshold value itself is unchanged. *Decreases membrane potential* - This phrasing is ambiguous. If "decreases" means becoming **more negative** (hyperpolarization), this is incorrect—hyperkalemia causes **depolarization** (less negative). - If "decreases" means the **absolute value decreases** (e.g., from -70 mV to -60 mV, moving toward 0), this could be correct but is poorly worded. - The preferred terminology is that hyperkalemia **depolarizes** the membrane or makes it **less negative**.

Question 9: Absolute refractoriness of a neuron is due to?

A. Hyperpolarization of Cl channels
B. Opening of rectifier K+ channels
C. Closure of activated Na channels
D. Inactivation of Na channels (Correct Answer)

Explanation: ***Inactivation of Na channels*** - During the **absolute refractory period**, voltage-gated **Na+ channels** enter an inactivated state, making them unresponsive to further stimulation. - This inactivation prevents another action potential from being generated, regardless of the stimulus intensity, ensuring unidirectional propagation. *Hyperpolarization of Cl channels* - While **Cl- channels** can cause hyperpolarization, this typically leads to **inhibition** rather than absolute refractoriness. - Their activity doesn't directly prevent the generation of a new action potential by blocking Na+ channel function. *Opening of rectifier K+ channels* - The opening of **rectifier K+ channels** is involved in **repolarization** and the **relative refractory period**, by increasing K+ efflux. - While it contributes to making the neuron less excitable, it doesn't cause the absolute inability to fire associated with Na+ channel inactivation. *Closure of activated Na channels* - The **closure of activated Na+ channels** occurs as part of the repolarization process, but the critical mechanism for absolute refractoriness is their transition into an **inactivated state**, not simply closure. - **Inactivation** locks the channels in a non-responsive configuration, whereas simple closure would allow them to reopen quickly with sufficient depolarization.

Question 10: Which of the following is NOT a characteristic of a biphasic action potential of a mixed nerve?

A. Refractory period
B. All or none phenomenon
C. Recorded on surface
D. Two or more positive peaks (Correct Answer)

Explanation: ***Two or more positive peaks*** - A **biphasic action potential** of a mixed nerve, when recorded extracellularly, typically consists of two phases: an initial **negative deflection** followed by a **positive deflection**. It does not exhibit multiple positive peaks for a single action potential. - The shape is determined by the propagation of the action potential past two recording electrodes, illustrating the **depolarization and repolarization** of the nerve. *All or none phenomenon* - This is a fundamental characteristic of **individual nerve fibers** and thus applies to the action potentials propagating within a mixed nerve. - If a stimulus reaches a threshold, a full-sized action potential is generated; otherwise, none is generated, regardless of stimulus strength. *Refractory period* - The **refractory period** is a crucial characteristic of nerve excitability, ensuring unidirectional propagation and limiting the frequency of action potentials. - This period, comprising absolute and relative phases, applies to the individual fibers within the mixed nerve. *Recorded on surface* - **Compound action potentials (CAPs)** of mixed nerves are typically recorded extracellularly (on the surface) using electrodes, often seen in nerve conduction studies. - This contrasts with intracellular recordings which measure the potential across the cell membrane directly.

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