Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 341: Sweating as a result of exertion is mediated through

A. Adrenal hormones
B. Parasympathetic cholinergic
C. Sympathetic adrenergic
D. Sympathetic cholinergic (Correct Answer)

Explanation: ***Sympathetic cholinergic*** - **Sweat glands**, primarily **eccrine glands**, are innervated by the **sympathetic nervous system**. - However, in this unique case, the postganglionic sympathetic fibers release **acetylcholine** (ACh) rather than norepinephrine, making them **cholinergic**. *Adrenal hormones* - While **catecholamines** like epinephrine and norepinephrine from the adrenal medulla can cause some sweating, it's typically a more generalized and stress-related response, not the primary mechanism for **exertional sweating**. - Adrenal hormones play a broader role in the **fight-or-flight response**, affecting various organs, but direct control over eccrine sweat glands is minimal compared to direct innervation. *Parasympathetic cholinergic* - The **parasympathetic nervous system** primarily uses **acetylcholine** as its neurotransmitter, but it generally leads to widespread systemic effects like **bronchoconstriction** and **bradycardia**. - This system is responsible for "rest and digest" functions and does not directly innervate **sweat glands** for thermoregulation. *Sympathetic adrenergic* - The majority of **sympathetic postganglionic neurons** release **norepinephrine**, making them adrenergic, which acts on alpha and beta receptors in target tissues. - While this system is crucial for cardiovascular regulation and other stress responses, it is not involved in directly stimulating **sweat glands** for thermoregulation.

Question 342: The protein responsible for elasticity of the muscle is:

A. Myosin
B. Titin (Correct Answer)
C. Actin
D. Tropomyosin

Explanation: ***Titin*** - **Titin** is a giant protein that functions as a molecular spring within the sarcomere, providing **passive elasticity** to muscle. - It helps anchor **myosin filaments** and contributes to the muscle's ability to **stretch and recoil**. *Myosin* - **Myosin** is primarily responsible for generating force and muscle contraction through its interaction with **actin**, not for elasticity. - It forms the thick filaments and uses **ATP hydrolysis** to power the cross-bridge cycle. *Actin* - **Actin** forms the thin filaments and serves as the binding site for myosin heads during muscle contraction. - While essential for contraction, it does not provide the primary elastic properties of muscle. *Tropomyosin* - **Tropomyosin** is a regulatory protein that wraps around actin filaments and blocks myosin-binding sites in the relaxed state. - It plays a role in **muscle contraction regulation**, not in providing elasticity.

Question 343: Find the true statement regarding sensory endings

A. Annulospiral wrap the ends
B. Primary ending is flower spray
C. Primary ending conduct 1b fibres
D. Flower spray is secondary (Correct Answer)

Explanation: ***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.

Question 344: Golgi tendon organ function is?

A. Detects the dynamic change in muscle length
B. Detects the muscle stretch
C. Detects the muscle strength
D. Detects the muscle tension (Correct Answer)

Explanation: ***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.

Question 345: 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 346: Acetylcholine release can be increased from presynaptic membrane by:

A. Blocking voltage gated K+ channels on presynaptic membrane (Correct Answer)
B. Blocking voltage gated Cl- channels on presynaptic membrane
C. Blocking voltage gated Na+ channels on presynaptic membrane
D. Blocking voltage gated Ca2+ channels on presynaptic membrane

Explanation: ***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.

Question 347: Which of the following neurotransmitters is primarily released from the sympathetic nervous system to increase heart rate in response to a DECREASE in blood pressure?

A. Norepinephrine (Correct Answer)
B. Dopamine
C. Acetylcholine
D. Epinephrine

Explanation: ***Norepinephrine*** - **Norepinephrine** is the primary neurotransmitter released by **postganglionic sympathetic neurons** directly onto the heart to increase heart rate and contractility in response to a drop in blood pressure. - It acts on **beta-1 adrenergic receptors** in the sinoatrial (SA) node, atria, and ventricles, leading to increased chronotropy (heart rate) and inotropy (contractility). *Dopamine* - While **dopamine** can have cardiovascular effects, particularly at high doses, it is not the primary neurotransmitter released by the sympathetic nervous system for direct heart rate regulation. - Dopamine is a precursor to norepinephrine and epinephrine, but its main physiological roles involve **renal blood flow regulation** and central nervous system functions. *Acetylcholine* - **Acetylcholine** is the primary neurotransmitter of the **parasympathetic nervous system**, which generally acts to **decrease heart rate** (bradycardia) through muscarinic receptors. - It is also released by **preganglionic sympathetic fibers**, but these do not directly innervate the heart to produce the desired effect of increasing heart rate. *Epinephrine* - **Epinephrine** (adrenaline) is primarily a **hormone** released from the **adrenal medulla** into the bloodstream, not directly from postganglionic sympathetic nerve terminals to the heart. - Although it has strong effects on beta-1 receptors in the heart, its release is more generalized and slower than the direct neuronal release of norepinephrine.

Question 348: What is the role of myelin in the nervous system?

A. Increase conduction speed (Correct Answer)
B. Increase synaptic delay
C. Increase capacitance
D. Decrease electrical resistance

Explanation: ***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.

Question 349: What is the neurotransmitter primarily involved in muscle contraction?

A. Glutamate
B. Acetylcholine (Correct Answer)
C. Dopamine
D. Serotonin

Explanation: ***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.

Question 350: Which enzyme degrades acetylcholine at the neuromuscular junction?

A. Acetylcholinesterase (Correct Answer)
B. Catechol-O-methyltransferase
C. Glutaminase
D. Monoamine oxidase

Explanation: ***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**.

Practice by Chapter

Resting Membrane Potential

Practice Questions

Action Potential Generation and Propagation

Practice Questions

Neuromuscular Junction

Practice Questions

Skeletal Muscle Contraction

Practice Questions

Smooth Muscle Physiology

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Cardiac Muscle Properties

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Muscle Metabolism and Fatigue

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Motor Unit Function

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Neurotransmitters and Receptors

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Electrophysiological Measurements

Practice Questions

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