Nerve and Muscle Physiology Practice Questions

Q: Which event will NOT occur during the depolarization phase?

K+ channels open. ### Explanation The correct answer is **C. K+ channels open**. #### 1. Underlying Medical Concept Depolarization is the phase of an action potential where the membrane potential becomes more positive (less negative). In a typical nerve or muscle cell, this is driven by the **influx of cations** (positive ions) into the cell. * **K+ channels** are primarily responsible for the **repolarization** phase. When K+ channels open, K+ ions exit the cell (efflux) along their concentration gradient, making the interior of the cell more negative again. Therefore, K+ channel opening is an event that follows depolarization, rather than occurring during it. #### 2. Analysis of Incorrect Options * **A. Na+ channels open:** This is the hallmark of the depolarization phase in neurons and skeletal muscle. Rapid opening of voltage-gated Na+ channels leads to a massive Na+ influx, causing the rapid upstroke of the action potential. * **B. Ca+ channels open:** In specific tissues, such as cardiac pacemaker cells (SA node) and smooth muscle, depolarization is mediated by the opening of voltage-gated Ca²+ channels. Even in ventricular myocytes, Ca²+ channels open during the late phase of depolarization to contribute to the plateau phase. #### 3. High-Yield Clinical Pearls for NEET-PG * **Threshold Potential:** The specific membrane potential (usually -55mV in nerves) at which voltage-gated Na+ channels open to trigger depolarization. * **Tetrodotoxin (TTX):** A potent neurotoxin (from Pufferfish) that blocks voltage-gated Na+ channels, preventing depolarization. * **Hyperkalemia:** Increases resting membrane potential (making it less negative), which initially makes cells more excitable but eventually leads to inactivation of Na+ channels, causing paralysis or arrhythmias. * **Absolute Refractory Period:** Occurs during depolarization and early repolarization when Na+ channels are either already open or in an inactivated state.

Q: Which one of the following muscle proteins plays an important role in the contraction of both smooth and striated muscle?

Actin. **Explanation:** The fundamental mechanism of muscle contraction in both striated (skeletal and cardiac) and smooth muscle is the **Sliding Filament Theory**. This process relies on the interaction between two primary contractile proteins: **Actin** (thin filament) and **Myosin** (thick filament). **Why Actin is the Correct Answer:** Actin is a highly conserved structural protein that forms the backbone of the thin filaments. Regardless of the muscle type, contraction cannot occur without the cross-bridge cycling between actin and myosin. While the regulatory mechanisms (how contraction is triggered) differ between muscle types, the physical "sliding" of actin over myosin is the universal final common pathway for tension generation. **Analysis of Incorrect Options:** * **Calmodulin (A):** This is the primary calcium-binding regulatory protein in **smooth muscle** only. It activates Myosin Light Chain Kinase (MLCK). It is not involved in striated muscle contraction, where calcium binds to Troponin C. * **Troponin (B):** This regulatory complex (consisting of Troponin I, T, and C) is unique to **striated muscle**. Smooth muscle lacks troponin entirely. * **Tropomyosin (C):** While tropomyosin is present in both, its role in smooth muscle is less clearly defined and not essential for the initiation of contraction in the same way it is for striated muscle (where it blocks the myosin-binding site on actin). **NEET-PG High-Yield Pearls:** * **Striated Muscle:** Regulation is **actin-linked** (via the Troponin-Tropomyosin complex). * **Smooth Muscle:** Regulation is **myosin-linked** (via phosphorylation of the Myosin Light Chain). * **Commonality:** Both require ATP and an increase in intracellular Calcium, though the source of calcium in smooth muscle is primarily extracellular/sarcolemmal, whereas in skeletal muscle, it is the Sarcoplasmic Reticulum.

Q: What are postganglionic sympathetic fibres?

C fibres. ### Explanation The classification of nerve fibres is a high-yield topic in neurophysiology, primarily based on the **Erlanger-Gasser classification**, which categorizes fibres according to their diameter, myelination, and conduction velocity. **Why C fibres are the correct answer:** Postganglionic sympathetic fibres are unique because they are **unmyelinated**. According to the Erlanger-Gasser classification, **Type C fibres** are the only unmyelinated fibres. They have the smallest diameter (0.4–1.2 μm) and the slowest conduction velocity (0.5–2.0 m/s). These fibres carry postganglionic autonomic signals and slow pain (prolonged, burning sensation). **Analysis of Incorrect Options:** * **Option A (A-alpha):** These are the largest, most heavily myelinated fibres. They function as somatic motor fibres (to extrafusal muscle fibres) and carry proprioception (from muscle spindles and Golgi tendon organs). * **Option C (B fibres):** These are small, lightly myelinated fibres. Crucially, they represent **preganglionic** autonomic fibres (both sympathetic and parasympathetic). * **Option D (A-gamma):** These are myelinated fibres that supply the intrafusal muscle fibres of the muscle spindle, regulating muscle tone. **NEET-PG High-Yield Pearls:** 1. **The "B" vs. "C" Rule:** Always remember: **B** comes before **C** in the alphabet, just as **Preganglionic (B)** comes before **Postganglionic (C)** in the autonomic pathway. 2. **Susceptibility:** * **Local Anesthetics:** Block **C fibres** first (smallest diameter). * **Pressure:** Affects **A fibres** first (largest diameter). * **Hypoxia:** Affects **B fibres** first. 3. **Fast vs. Slow Pain:** Fast pain is carried by **A-delta** fibres, while slow, chronic pain is carried by **C fibres**.

Q: After an injury to an axon, the subsequent degeneration of all axonal fibres distal to the injury, with all fibres proximal to the injury remaining unaffected, is known as which type of degeneration?

Wallerian degeneration.. **Explanation:** **Wallerian Degeneration (Orthograde Degeneration)** refers to the pathological changes that occur in the **distal segment** of an axon following a traumatic injury or transection. Since the distal portion is separated from the neuronal cell body (the metabolic center), it loses its supply of essential proteins and nutrients. This leads to the disintegration of the axon and the breakdown of the myelin sheath, which are subsequently cleared by macrophages and Schwann cells. **Analysis of Incorrect Options:** * **Retrograde Degeneration:** This refers to pathological changes occurring **proximal** to the site of injury (towards the cell body). It involves the breakdown of the axon up to the first node of Ranvier and characteristic changes in the cell body known as *chromatolysis* (swelling of the cell body and displacement of the nucleus). * **Transneuronal Degeneration:** This occurs when the death of one neuron leads to the degeneration of another neuron with which it synapses. It can be anterograde (affecting the postsynaptic neuron) or retrograde (affecting the presynaptic neuron). **High-Yield NEET-PG Pearls:** * **Chromatolysis:** The hallmark of retrograde degeneration in the cell body; involves the disappearance of Nissl granules (RER). * **Regeneration:** In the Peripheral Nervous System (PNS), Schwann cells form **Bungner bands**, which act as physical guides for regenerating axonal sprouts. * **Rate of Growth:** Regenerating nerve fibers typically grow at a rate of **1–4 mm/day**. * **Blood-Brain Barrier:** Wallerian degeneration is slower in the CNS compared to the PNS because oligodendrocytes do not provide the same growth-promoting environment as Schwann cells.

Q: The thick filament is primarily composed of which of the following?

Heavy chain of myosin and Light chain of myosin. **Explanation:** The sarcomere is the functional unit of skeletal muscle, consisting of thick and thin filaments. The **thick filament** is composed almost entirely of the protein **myosin**. A single myosin molecule is a hexamer consisting of **two heavy chains** and **four light chains**. * **Heavy Chains:** These coil together to form the "tail" (rod) and the globular "heads." The heads possess ATPase activity and the actin-binding site necessary for cross-bridge cycling. * **Light Chains:** Two pairs of light chains (alkali and regulatory) wrap around the "neck" region of the heavy chains, providing structural stability and modulating the velocity of muscle contraction. **Analysis of Incorrect Options:** * **Dystrophin:** This is a large cytoskeletal protein that links the intracellular actin cytoskeleton to the extracellular matrix (via the dystroglycan complex). It is not a component of the thick filament itself. * **Titin:** Known as the largest protein in the body, titin acts as a molecular spring that anchors the thick filament to the Z-disk. While it interacts with the thick filament to maintain its central position, it is considered an **accessory/structural protein**, not a primary constituent of the thick filament. **NEET-PG High-Yield Pearls:** * **Thin Filaments:** Composed of Actin, Tropomyosin, and Troponin (C, I, and T). * **H-Zone:** The central region of the A-band that contains **only** thick filaments (no actin overlap). * **Clinical Correlation:** Mutations in the **Dystrophin** gene lead to Duchenne and Becker Muscular Dystrophies. * **M-Line:** The structural protein **Myomesin** anchors the thick filaments at the center of the sarcomere.

Q: Which of the following statements regarding skeletal and cardiac muscle is false?

Both have graded contractions.. ### Explanation The correct answer is **C**, as the statement "Both have graded contractions" is false. **1. Why Option C is False (The Correct Answer):** Skeletal muscle fibers follow the **"All-or-None Law"** at the cellular level. However, the muscle as a whole can produce graded contractions through motor unit recruitment and frequency summation. In contrast, **cardiac muscle** functions as a **functional syncytium** due to gap junctions in intercalated discs. When one cell is excited, the entire myocardium contracts as a single unit. Therefore, cardiac muscle cannot recruit additional motor units; it follows the all-or-none law for the entire organ, making "graded contractions" (in the sense of recruitment) impossible for the heart. **2. Analysis of Incorrect Options:** * **Option A:** Both muscles require calcium to bind to **Troponin C**, which moves tropomyosin and allows actin-myosin cross-bridge formation. * **Option B:** In skeletal muscle, the Dihydropyridine (DHP) receptor acts as a voltage sensor physically coupled to the Ryanodine receptor (RyR1). It triggers calcium release from the Sarcoplasmic Reticulum (SR) without needing extracellular calcium influx. Thus, it is independent of extracellular $Ca^{2+}$. * **Option D:** Cardiac muscle has a prolonged **Plateau Phase (Phase 2)** caused by the opening of L-type $Ca^{2+}$ channels, which prevents tetany and allows for adequate ventricular filling. **High-Yield NEET-PG Pearls:** * **Trigger for $Ca^{2+}$ release:** In skeletal muscle, it is **Voltage-gated** (electromechanical coupling). In cardiac muscle, it is **Calcium-Induced Calcium Release (CICR)** via RyR2. * **Refractory Period:** Cardiac muscle has a very long absolute refractory period (250ms), making it **impossible to tetanize**, unlike skeletal muscle. * **Source of $Ca^{2+}$:** Skeletal muscle relies 100% on the SR; Cardiac muscle relies on both the SR and extracellular fluid (ECF).

Q: What is the threshold level for a neuronal action potential?

-55 mV. **Explanation:** The **threshold potential** is the critical membrane voltage to which a nerve cell must be depolarized to initiate an action potential. In a typical neuron, this value is approximately **-55 mV**. 1. **Why -55 mV is correct:** At the resting membrane potential (RMP) of -70 mV, voltage-gated sodium (Na⁺) channels are closed. When a stimulus depolarizes the membrane to -55 mV, it reaches the "point of no return." At this threshold, the activation gates of voltage-gated Na⁺ channels open rapidly, leading to a massive influx of Na⁺ ions. This creates a positive feedback loop (Hodgkin cycle), resulting in the rapid upstroke of the action potential. 2. **Analysis of Incorrect Options:** * **-70 mV (Option A):** This is the typical **Resting Membrane Potential (RMP)** of a neuron, where the cell is at electrical equilibrium and no action potential is firing. * **+70 mV (Option B):** This value is physiologically irrelevant for neuronal thresholds; it is far beyond the equilibrium potential for sodium. * **+55 mV (Option D):** This is the **Equilibrium Potential for Sodium (ENa⁺)**. During the peak of an action potential, the membrane potential approaches but never quite reaches this value. **High-Yield NEET-PG Pearls:** * **All-or-None Law:** If the threshold (-55 mV) is reached, an action potential of constant amplitude occurs. If it is not reached, no action potential occurs. * **Hypocalcemia:** Increases neuronal excitability by lowering the threshold (making it more negative/closer to RMP), leading to tetany. * **Hypercalcemia:** Decreases excitability by raising the threshold (making it less negative/further from RMP). * **Accommodation:** A slow, gradual depolarization can cause the threshold to rise, preventing an action potential from firing despite reaching the usual -55 mV level.

Q: In the length-tension relationship of skeletal muscle, what is the length at which active tension is maximum?

Sarcomere length 2.25 micrometers. **Explanation:** The length-tension relationship in skeletal muscle is governed by the **Sliding Filament Theory**. Active tension is directly proportional to the number of **cross-bridge formations** between actin (thin) and myosin (thick) filaments. **1. Why Option D is Correct:** The maximum active tension is achieved at the **optimal sarcomere length ($L_0$)**, which ranges between **2.0 and 2.25 $\mu$m**. At 2.25 $\mu$m, there is an ideal overlap between actin and myosin, allowing the maximum number of cross-bridges to form. This results in the peak of the length-tension curve. **2. Why Other Options are Incorrect:** * **Option B (3.65 $\mu$m):** This is the point of **zero active tension**. At this length, the sarcomere is stretched so far that actin and myosin filaments do not overlap at all; hence, no cross-bridges can form. * **Option C (1.65 $\mu$m):** At this shortened length, the actin filaments from opposite ends of the sarcomere begin to overlap and collide (interference), and the thick myosin filaments hit the Z-discs. This physical crowding significantly reduces tension. * **Option A (2.0 $\mu$m):** While 2.0 $\mu$m is the lower limit of the "plateau" of maximum tension, 2.25 $\mu$m is the standard physiological value cited for the peak of the length-tension relationship in most medical textbooks (like Guyton). **High-Yield Facts for NEET-PG:** * **Total Tension:** The sum of Active Tension (cross-bridge cycling) and Passive Tension (elastic recoil of titin and connective tissue). * **Frank-Starling Law:** This is the cardiac application of the length-tension relationship, though cardiac muscle operates on the ascending limb of the curve to prevent overstretching. * **Titin:** The protein responsible for the **passive tension** in a muscle fiber.

Q: Which one of the following is a regulatory protein of the muscle?

Troponin. **Explanation:** The contractile machinery of skeletal muscle is composed of three functional categories of proteins: contractile, regulatory, and structural. **1. Why Troponin is Correct:** **Troponin** and **Tropomyosin** are the primary **regulatory proteins**. In a resting state, tropomyosin covers the myosin-binding sites on the actin filament. Troponin consists of three subunits: * **Troponin C:** Binds to Calcium ions. * **Troponin I:** Inhibits the actin-myosin interaction. * **Troponin T:** Tethers the troponin complex to tropomyosin. When $Ca^{2+}$ binds to Troponin C, a conformational change occurs that moves tropomyosin away, allowing the "power stroke" to occur. **2. Why the Other Options are Incorrect:** * **Myosin (Option B):** This is a **contractile protein** (thick filament). It possesses ATPase activity and forms cross-bridges with actin. * **Actin (Option C):** This is a **contractile protein** (thin filament). It provides the binding sites for myosin heads. * **Protein-C (Option D):** This is a physiological **anticoagulant** synthesized in the liver (Vitamin K dependent). It is not a structural or regulatory component of the muscle sarcomere. **High-Yield NEET-PG Pearls:** * **Sarcomere:** The functional unit of contraction, defined as the segment between two Z-lines. * **Dystrophin:** A vital structural protein; its deficiency leads to Duchenne Muscular Dystrophy. * **Titin:** The largest protein in the body; it acts as a molecular spring providing passive elasticity to the muscle. * **Clinical Marker:** Cardiac Troponin I and T are highly specific gold-standard biomarkers for diagnosing Myocardial Infarction (MI).

Question 1

Which event will NOT occur during the depolarization phase?

Accepted Answer

K+ channels open

Answer

Na+ channels open

Answer

Ca+ channels open

Answer

None of the above

Question 2

Which one of the following muscle proteins plays an important role in the contraction of both smooth and striated muscle?

Accepted Answer

Actin

Answer

Calmodulin

Answer

Troponin

Answer

Tropomyosin

Question 3

The length of a muscle at which tension is maximum is called:

Accepted Answer

Optimal length

Answer

Active length

Answer

Resting length

Answer

Maximal length

Question 4

What are postganglionic sympathetic fibres?

Accepted Answer

C fibres

Answer

A alpha fibres

Answer

B fibres

Answer

A gamma fibres

Question 5

After an injury to an axon, the subsequent degeneration of all axonal fibres distal to the injury, with all fibres proximal to the injury remaining unaffected, is known as which type of degeneration?

Accepted Answer

Wallerian degeneration.

Answer

Retrograde degeneration.

Answer

Transneuronal degeneration.

Answer

None of the above.

Question 6

The thick filament is primarily composed of which of the following?

Accepted Answer

Heavy chain of myosin and Light chain of myosin

Answer

Heavy chain of myosin, Dystrophin, and Titin

Answer

Light chain of myosin, Dystrophin, and Titin

Answer

Dystrophin and Titin

Question 7

Which of the following statements regarding skeletal and cardiac muscle is false?

Accepted Answer

Both have graded contractions.

Answer

Both require calcium for excitation-contraction coupling.

Answer

The excitation-contraction coupling of skeletal muscle is independent of extracellular calcium.

Answer

A plateau phase is seen in the action potential of cardiac muscle.

Question 8

What is the threshold level for a neuronal action potential?

Accepted Answer

-55 mV

Answer

-70 mV

Answer

+70 mV

Answer

+55 mV

Question 9

In the length-tension relationship of skeletal muscle, what is the length at which active tension is maximum?

Accepted Answer

Sarcomere length 2.25 micrometers

Answer

Sarcomere length 2.0 micrometers

Answer

Sarcomere length 3.65 micrometers

Answer

Sarcomere length 1.65 micrometers

Question 10

Which one of the following is a regulatory protein of the muscle?

Accepted Answer

Troponin

Answer

Myosin

Answer

Actin

Answer

Protein-C

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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