Nerve and Muscle Physiology Practice Questions

Q: The Nernst potential of K+ is (in mV):

-90. ***-90*** - The **Nernst potential** for K+ is approximately -90 mV, the standard textbook value used in medical education, calculated using the Nernst equation with typical intracellular (140 mEq/L) and extracellular (4 mEq/L) concentrations of K+. - This value represents the **equilibrium potential** at which there is no net movement of potassium ions across the cell membrane. - This rounded value is consistently cited in standard physiology texts (Ganong, Guyton) and is the expected answer for medical examinations. *-10* - This value is significantly less negative than the actual Nernst potential for K+ and does not reflect the typical concentration gradient of potassium. - An equilibrium potential of -10 mV would imply a much smaller concentration gradient or a different ion species. *-61* - This value is close to the typical **resting membrane potential** of many excitable cells (around -70 mV), but not the Nernst potential for K+ specifically. - The resting membrane potential is a weighted average of the Nernst potentials of several ions, with K+ being a major contributor due to its high permeability. *-94* - While this represents a more precise calculation using the Nernst equation, **-90 mV is the standard textbook value** taught in medical physiology and expected in examinations. - The difference between -90 and -94 mV reflects rounding conventions; -90 mV is universally accepted in clinical and academic contexts.

Q: Find the true statement regarding sensory endings

Flower spray is secondary. ***Flower spray is secondary*** - The flower spray endings refer to the **secondary sensory endings** of the muscle spindle, which are located primarily on the **nuclear chain fibers**. - These endings detect changes in **muscle length** and respond more proportionally to static stretch. *Annulospiral wrap the ends* - The annulospiral endings are the **primary sensory endings** of the muscle spindle. - They are located in the **central/equatorial portion** of the intrafusal fibers (not the ends) and respond to both the **rate** and **degree** of muscle stretch. *Primary ending is flower spray* - The primary endings are known as **annulospiral endings**, not flower spray. - Flower spray endings refer to the secondary sensory endings, which have a different morphology and functional response. *Primary ending conduct 1b fibres* - Primary endings of muscle spindles conduct **Ia afferent fibers**, which are large, myelinated, and rapidly conducting. - **Ib afferent fibers** originate from **Golgi tendon organs**, which sense muscle tension, not muscle length changes detected by primary spindle endings.

Q: Golgi tendon organ function is?

Detects the muscle tension. ***Detects the muscle tension*** - The **Golgi tendon organ (GTO)** is a proprioceptor located at the musculotendinous junction, specifically designed to monitor and respond to changes in **muscle tension** or force. - When muscle tension increases, such as during a strong contraction, the GTO sends inhibitory signals to the motor neurons of the same muscle, leading to muscle relaxation and preventing injury (autogenic inhibition). *Detects the dynamic change in muscle length* - This function is primarily attributed to **muscle spindles**, which are specialized sensory receptors that detect changes in the **length** and rate of change of length of a muscle. - Muscle spindles are responsible for the **stretch reflex**, initiating a contraction when a muscle is stretched too quickly. *Detects the muscle stretch* - While GTOs are involved in reflex responses that can follow muscle stretch, their primary role is not to detect the stretching itself, but rather the **tension** that results from that stretch. - **Muscle spindles** are the primary mechanoreceptors responsible for detecting the stretch of a muscle. *Detects the muscle strength* - "Muscle strength" is a broader term referring to the force a muscle can exert, which is controlled by a combination of neural input and muscle fiber characteristics. - While GTOs contribute to the overall proprioceptive feedback regulating muscle force, they specifically detect **tension** rather than directly measuring "strength" as a global concept.

Q: Absolute refractoriness of a neuron is due to?

Inactivation of Na channels. ***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.

Q: Acetylcholine release can be increased from presynaptic membrane by:

Blocking voltage gated K+ channels on presynaptic membrane. ***Blocking voltage gated K+ channels on presynaptic membrane*** - Blocking **voltage-gated K+ channels** prevents repolarization, prolonging the **action potential** duration and keeping the presynaptic membrane depolarized for a longer time. - This extended depolarization leads to increased opening of **voltage-gated Ca2+ channels**, allowing more Ca2+ influx and thus enhancing **acetylcholine release**. *Blocking voltage gated Cl- channels on presynaptic membrane* - **Chloride channels** primarily contribute to establishing the **resting membrane potential** or mediating inhibitory postsynaptic potentials, and their direct blocking does not primarily enhance acetylcholine release. - An increase in intracellular Cl- concentration could lead to depolarization, but specific voltage-gated Cl- channels are not the primary regulators of **neurotransmitter release**. *Blocking voltage gated Na+ channels on presynaptic membrane* - **Voltage-gated Na+ channels** are essential for the **initiation and propagation of action potentials**; blocking them would prevent depolarization. - Preventing depolarization would inhibit, rather than increase, the opening of voltage-gated Ca2+ channels and subsequently **acetylcholine release**. *Blocking voltage gated Ca2+ channels on presynaptic membrane* - **Voltage-gated Ca2+ channels** are directly responsible for the influx of Ca2+ into the presynaptic terminal, which is the crucial trigger for **neurotransmitter release**. - Blocking these channels would **reduce or abolish Ca2+ influx**, thereby *decreasing* rather than increasing acetylcholine release.

Q: What is the role of myelin in the nervous system?

Increase conduction speed. ***Increase conduction speed*** - Myelin forms an electrical insulator around the axon, preventing ion leakage and allowing **saltatory conduction**. - This **saltatory conduction** means the action potential 'jumps' between nodes of Ranvier, significantly increasing the speed of nerve impulse transmission. *Increase synaptic delay* - Myelin's role is in **axonal conduction**, not synaptic transmission. An increase in synaptic delay would slow down overall communication. - The delay at the synapse is primarily due to the time required for neurotransmitter release, diffusion, and receptor binding. *Increase capacitance* - Myelin actually **decreases membrane capacitance** while increasing electrical resistance. - A lower capacitance allows the membrane potential to change more quickly in response to current flow, contributing to faster conduction. *Decrease electrical resistance* - Myelin actually **increases electrical resistance** (transverse resistance) of the axonal membrane, not decreases it. - This high resistance prevents current from leaking out across the membrane, forcing it to flow longitudinally down the axon, which is essential for saltatory conduction and rapid signal propagation.

Q: How does myasthenia gravis cause muscle weakness?

Blocks ACh receptors at the neuromuscular junctions.. ***Blocks ACh receptors at the neuromuscular junctions.*** - Myasthenia gravis is an **autoimmune disorder** where the body produces **antibodies** that target and block the **nicotinic acetylcholine receptors (AChRs)** at the **neuromuscular junction** [1]. - This blocking prevents acetylcholine from binding effectively to the muscle cell, leading to a **reduced number of available receptors** and thus impaired muscle contraction and characteristic **muscle weakness** [2]. *Increases acetylcholine degradation.* - An increase in **acetylcholine degradation** would mean that **acetylcholinesterase** is overly active, breaking down acetylcholine more quickly. - While this would reduce available acetylcholine, it is **not the primary mechanism** in myasthenia gravis, where the issue is primarily with the receptors themselves [2]. *Inhibits acetylcholine release.* - Conditions like **Lambert-Eaton myasthenic syndrome (LEMS)**, not myasthenia gravis, are characterized by antibodies targeting **presynaptic voltage-gated calcium channels**, leading to **reduced acetylcholine release** [3]. - In myasthenia gravis, acetylcholine is released normally from the presynaptic neuron, but it cannot bind to the blocked receptors. *Decreases acetylcholine production.* - A decrease in acetylcholine production would imply a problem in the **synthesis of the neurotransmitter**, which is typically performed in the presynaptic neuron. - Myasthenia gravis does not primarily affect the production of acetylcholine; rather, it affects the **postsynaptic response** to acetylcholine.

Q: What is the neurotransmitter primarily involved in muscle contraction?

Acetylcholine. ***Acetylcholine*** - **Acetylcholine (ACh)** acts at the **neuromuscular junction** to initiate muscle contraction by binding to nicotinic receptors on the muscle fiber membrane. - This binding causes depolarization and triggers the release of **calcium** from the sarcoplasmic reticulum, essential for the interaction of actin and myosin filaments. *Glutamate* - **Glutamate** is the primary **excitatory neurotransmitter** in the central nervous system, mainly involved in synaptic transmission, learning, and memory. - It does not mediate signal transmission at the **neuromuscular junction** for skeletal muscle contraction. *Dopamine* - **Dopamine** is a neurotransmitter involved in reward, motivation, and motor control pathways within the **central nervous system** (basal ganglia). - It does not play a direct role in the peripheral process of **skeletal muscle contraction** at the neuromuscular junction. *Serotonin* - **Serotonin** primarily regulates mood, sleep, appetite, and gastrointestinal function in the **central nervous system**. - It is not involved in directly signaling **skeletal muscle fibers** for contraction at the neuromuscular junction.

Q: Which enzyme degrades acetylcholine at the neuromuscular junction?

Acetylcholinesterase. ***Acetylcholinesterase*** - This enzyme is located in the **synaptic cleft** and rapidly **hydrolyzes acetylcholine** into acetate and choline, terminating its action. - Its efficient degradation of acetylcholine ensures precise control over muscle contraction and relaxation at the **neuromuscular junction**. *Catechol-O-methyltransferase* - This enzyme is primarily involved in the degradation of **catecholamines** like dopamine, norepinephrine, and epinephrine, not acetylcholine. - It plays a significant role in the metabolism of neurotransmitters in the **central nervous system** and peripheral tissues, but not specifically at the neuromuscular junction for acetylcholine. *Glutaminase* - This enzyme is responsible for converting **glutamine to glutamate**, a crucial step in the synthesis of the excitatory neurotransmitter glutamate. - It is not involved in the degradation of acetylcholine at any synapse. *Monoamine oxidase* - This enzyme metabolizes **monoamine neurotransmitters** such as serotonin, dopamine, and norepinephrine, primarily within the synapse. - It does not act on acetylcholine, which is a **cholinergic neurotransmitter**.

Q: A patient experiences sudden muscle weakness after consuming a large amount of potassium-rich food. Which physiological mechanism is likely responsible for the muscle weakness?

Depolarization of the nerve membrane. ***Depolarization of the nerve membrane*** - A large intake of potassium-rich food can lead to **hyperkalemia**, causing the **resting membrane potential** of nerve and muscle cells to become less negative (depolarized). - While initial depolarization can fire action potentials, sustained depolarization inactivates **voltage-gated sodium channels**, preventing further firing and leading to **muscle weakness** or paralysis. *Decreased potassium efflux* - In situations of hyperkalemia, there might be a *relative* decrease in potassium efflux compared to the elevated extracellular potassium, but the primary mechanism leading to weakness is due to the sustained depolarization of the membrane. - Reduced potassium efflux wouldn't directly cause muscle weakness; rather, it would contribute to the inability to repolarize effectively. *Increased sodium influx* - While depolarization is linked to sodium channel function, the underlying issue in hyperkalemia leading to weakness is the sustained depolarization that inactivates these channels, not an increased sodium influx itself. - An uncontrolled increase in sodium influx would typically lead to increased excitability, not weakness, unless it's part of a cycle that inactivates voltage-gated channels. *Hyperpolarization of the nerve membrane* - **Hyperpolarization** would make the nerve membrane more negative and *less* excitable, eventually leading to muscle weakness by making it harder to reach the threshold for an action potential. - However, **hyperkalemia** causes **depolarization** (less negative resting membrane potential), making this option incorrect for the given scenario.

Question 1

The Nernst potential of K+ is (in mV):

Accepted Answer

-90

Answer

-10

Answer

-61

Answer

-94

Question 2

Find the true statement regarding sensory endings

Accepted Answer

Flower spray is secondary

Answer

Annulospiral wrap the ends

Answer

Primary ending is flower spray

Answer

Primary ending conduct 1b fibres

Question 3

Golgi tendon organ function is?

Accepted Answer

Detects the muscle tension

Answer

Detects the dynamic change in muscle length

Answer

Detects the muscle stretch

Answer

Detects the muscle strength

Question 4

Absolute refractoriness of a neuron is due to?

Accepted Answer

Inactivation of Na channels

Answer

Hyperpolarization of Cl channels

Answer

Opening of rectifier K+ channels

Answer

Closure of activated Na channels

Question 5

Acetylcholine release can be increased from presynaptic membrane by:

Accepted Answer

Blocking voltage gated K+ channels on presynaptic membrane

Answer

Blocking voltage gated Cl- channels on presynaptic membrane

Answer

Blocking voltage gated Na+ channels on presynaptic membrane

Answer

Blocking voltage gated Ca2+ channels on presynaptic membrane

Question 6

What is the role of myelin in the nervous system?

Accepted Answer

Increase conduction speed

Answer

Increase synaptic delay

Answer

Increase capacitance

Answer

Decrease electrical resistance

Question 7

How does myasthenia gravis cause muscle weakness?

Accepted Answer

Blocks ACh receptors at the neuromuscular junctions.

Answer

Increases acetylcholine degradation.

Answer

Inhibits acetylcholine release.

Answer

Decreases acetylcholine production.

Question 8

What is the neurotransmitter primarily involved in muscle contraction?

Accepted Answer

Acetylcholine

Answer

Glutamate

Answer

Dopamine

Answer

Serotonin

Question 9

Which enzyme degrades acetylcholine at the neuromuscular junction?

Accepted Answer

Acetylcholinesterase

Answer

Catechol-O-methyltransferase

Answer

Glutaminase

Answer

Monoamine oxidase

Question 10

A patient experiences sudden muscle weakness after consuming a large amount of potassium-rich food. Which physiological mechanism is likely responsible for the muscle weakness?

Accepted Answer

Depolarization of the nerve membrane

Answer

Decreased potassium efflux

Answer

Increased sodium influx

Answer

Hyperpolarization of the nerve membrane

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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