Nerve and Muscle Physiology Practice Questions

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).

Q: Which protein in muscle aids in relaxation?

Titin. **Explanation:** The correct answer is **Titin** (also known as connectin). Titin is the largest known protein in the human body and acts as a molecular spring within the sarcomere. It extends from the Z-disk to the M-line, anchoring the thick (myosin) filaments. During muscle contraction, titin stores elastic potential energy; once the contraction stimulus ceases, this stored energy provides the **passive recoil force** necessary to return the sarcomere to its resting length, thereby aiding in muscle relaxation. **Analysis of Incorrect Options:** * **Nebulin (A):** An actin-binding protein that acts as a "molecular ruler." It regulates the length of thin filaments during assembly but does not provide elastic recoil. * **Desmin (B):** A type III intermediate filament that links Z-disks of adjacent myofibrils to each other and to the plasma membrane. It maintains structural integrity and alignment rather than facilitating relaxation. * **Calcineurin (D):** A calcium-dependent phosphatase involved in signaling pathways (e.g., T-cell activation and muscle fiber type switching). It is an enzyme, not a structural protein involved in the mechanical recoil of the sarcomere. **High-Yield NEET-PG Pearls:** * **Titin:** Mutations in the *TTN* gene are a leading cause of **Dilated Cardiomyopathy (DCM)**. * **Dystrophin:** Often confused with these proteins, it links the cytoskeleton of a muscle fiber to the surrounding extracellular matrix (defective in Duchenne Muscular Dystrophy). * **Tropomyosin:** In the resting state, it covers the myosin-binding sites on actin, preventing contraction. Relaxation requires the re-uptake of $Ca^{2+}$ into the sarcoplasmic reticulum by **SERCA** pumps.

Q: All of the following are features of cardiac muscle EXCEPT:

Caldesmon is an important regulatory protein. **Explanation:** The correct answer is **D**. **Caldesmon** is a regulatory protein found specifically in **smooth muscle**, not cardiac muscle. It functions by binding to actin and tropomyosin, thereby inhibiting the ATPase activity of myosin and preventing contraction. In smooth muscle, contraction is initiated when calcium-calmodulin binds to caldesmon, releasing it from actin. **Analysis of Options:** * **A. Striated:** Cardiac muscle, like skeletal muscle, contains highly organized sarcomeres (the functional units of contraction), which give it a characteristic striated appearance under a microscope. * **B. Large T tubules:** Cardiac muscle features T-tubules that are significantly wider (up to 5 times the diameter) than those in skeletal muscle. They are located at the **Z-discs** (unlike skeletal muscle, where they are at the A-I junction). * **C. Troponin system present:** Cardiac contraction is regulated by the troponin complex (TnC, TnI, and TnT). Calcium binds to **Troponin C**, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiac Biomarkers:** Cardiac-specific isoforms of **Troponin I and T** are the gold-standard markers for diagnosing Myocardial Infarction (MI). * **Triads vs. Diads:** Skeletal muscle has "Triads" (1 T-tubule + 2 terminal cisternae), while cardiac muscle typically has **"Diads"** (1 T-tubule + 1 terminal cisterna). * **Smooth Muscle Regulation:** Remember that smooth muscle lacks troponin. Instead, it uses **Caldesmon, Calponin,** and the **Calmodulin-MLCK** (Myosin Light Chain Kinase) pathway.

Q: Initiation of nerve impulse occurs at the axon hillock because:

It has a lower threshold than the rest of the axon. The **axon hillock** (specifically the initial segment) is known as the **"Trigger Zone"** of the neuron. ### Why Option A is Correct The initiation of an action potential depends on the density of **voltage-gated sodium (Na+) channels**. The axon hillock has the highest concentration of these channels per unit area compared to the cell body or the rest of the axon. Because there are more channels available to open in response to depolarization, the **threshold for excitation is significantly lower** (approx. -45 mV) compared to the soma (approx. -30 mV). This makes it the site with the highest excitability, where graded potentials are summed to trigger an all-or-nothing impulse. ### Why Other Options are Incorrect * **Option B:** While the axon hillock is unmyelinated, this is not the functional reason for impulse *initiation*. Many parts of a neuron (like the dendrites and soma) are unmyelinated but cannot initiate an action potential as easily because they lack the necessary density of Na+ channels. * **Option C:** Neurotransmitter release occurs at the **axon terminals** (presynaptic boutons), not the hillock. The hillock is responsible for signal *generation*, while the terminal is responsible for signal *transmission*. ### High-Yield Facts for NEET-PG * **Initial Segment:** The actual site of impulse generation is the unmyelinated segment between the axon hillock and the first myelin sheath. * **Refractory Period:** This period is determined by the inactivation gate (h-gate) of the voltage-gated Na+ channels. * **Accommodation:** If a nerve is subjected to a slowly rising subthreshold stimulus, the threshold for firing increases; this is called accommodation. * **Safety Factor:** The ratio of action potential strength to the excitability threshold. In normal nerve fibers, this is usually greater than 1.

Question 1

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 2

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 3

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 4

What is the threshold level for a neuronal action potential?

Accepted Answer

-55 mV

Answer

-70 mV

Answer

+70 mV

Answer

+55 mV

Question 5

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 6

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

Accepted Answer

Troponin

Answer

Myosin

Answer

Actin

Answer

Protein-C

Question 7

Which protein in muscle aids in relaxation?

Accepted Answer

Titin

Answer

Nebulin

Answer

Desmin

Answer

Calcineurin

Question 8

Increase in cytosolic calcium from intracellular storage, during smooth muscle contraction is/are due to?

Accepted Answer

IP3-DAG

Answer

CAMP

Answer

CGMP

Answer

CCMP

Question 9

All of the following are features of cardiac muscle EXCEPT:

Accepted Answer

Caldesmon is an important regulatory protein

Answer

Striated

Answer

Large T tubules

Answer

Troponin system present

Question 10

Initiation of nerve impulse occurs at the axon hillock because:

Accepted Answer

It has a lower threshold than the rest of the axon

Answer

It is unmyelinated

Answer

Neurotransmitter release occurs here

Answer

None of the above

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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