Nerve and Muscle Physiology Practice Questions

Q: NN Nicotinic acetylcholine receptors are present on which of the following structures?

Presynaptic glutamate-secreting axon terminals. **Explanation:** Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels categorized into two main subtypes: **$N_M$ (Muscle-type)** and **$N_N$ (Neuronal-type)**. **Why Option C is Correct:** $N_N$ receptors are primarily found in the central nervous system (CNS) and autonomic ganglia. In the CNS, they are frequently located on **presynaptic terminals** of non-cholinergic neurons (such as glutamate-secreting axons). When acetylcholine binds to these presynaptic $N_N$ receptors, it triggers an influx of $Ca^{2+}$, which facilitates the release of other neurotransmitters like glutamate, dopamine, or norepinephrine. This is a key mechanism of neuromodulation in the brain. **Analysis of Incorrect Options:** * **Options B & D (Motor endplates / Neuromuscular junction):** These contain **$N_M$ receptors**, not $N_N$. While both are nicotinic, $N_M$ receptors have a different subunit composition ($\alpha_1, \beta_1, \delta, \epsilon/\gamma$) and are specifically targeted by muscle relaxants like succinylcholine or vecuronium. * **Option A (Myocardium):** The heart contains **Muscarinic ($M_2$) receptors**, which are G-protein coupled receptors (GPCRs), not nicotinic ion channels. Activation of $M_2$ receptors leads to a decrease in heart rate (negative chronotropy). **High-Yield Facts for NEET-PG:** * **$N_N$ Location:** Autonomic ganglia (both sympathetic and parasympathetic), adrenal medulla, and CNS. * **$N_N$ Blockers:** Hexamethonium and Trimethaphan (Ganglionic blockers). * **$N_M$ Blockers:** d-Tubocurarine (Competitive) and Succinylcholine (Depolarizing). * **Key Difference:** $N_N$ receptors are primarily involved in ganglionic transmission and neurotransmitter modulation, whereas $N_M$ receptors mediate skeletal muscle contraction.

Q: Which of the following statements is NOT true regarding Type 1 muscle fibers?

High glycolytic capacity. **Explanation:** Type 1 muscle fibers, also known as **Slow-Twitch (Red) fibers**, are specialized for endurance and aerobic metabolism. **1. Why Option A is the Correct Answer (NOT true):** Type 1 fibers have a **low glycolytic capacity**. They rely primarily on oxidative phosphorylation (aerobic metabolism) rather than glycolysis (anaerobic metabolism) to generate ATP. High glycolytic capacity is a hallmark of **Type 2 (Fast-Twitch/White) fibers**, which are designed for short bursts of powerful activity and fatigue quickly. **2. Why the other options are incorrect (True for Type 1):** * **High capillary density (Option B):** To support continuous aerobic metabolism, Type 1 fibers require a rich blood supply for the steady delivery of oxygen and nutrients. * **High number of mitochondria (Option C):** Mitochondria are the sites of the Krebs cycle and the electron transport chain; their high density in Type 1 fibers facilitates efficient ATP production over long periods. * **High myoglobin content (Option D):** Myoglobin is an iron-binding protein that stores oxygen within the muscle. Its high concentration gives these fibers their characteristic red color and ensures oxygen availability during sustained contraction. **High-Yield NEET-PG Pearls:** * **Mnemonic:** **"One Slow Red Ox"** (Type **1**, **Slow**-twitch, **Red** color, **Ox**idative metabolism). * **Fatigability:** Type 1 fibers are highly resistant to fatigue (e.g., soleus, back muscles for posture), whereas Type 2B fibers fatigue rapidly. * **ATPase Activity:** Type 1 fibers have low myosin ATPase activity, leading to a slower velocity of contraction compared to Type 2. * **Lipid Content:** Type 1 fibers have higher triglyceride stores, while Type 2 fibers have higher glycogen stores.

Q: Each myosin molecule of a sarcomere is composed of how many monomers?

Six monomers. **Explanation:** The correct answer is **Six monomers (Option C)**. Myosin II, the type found in skeletal muscle, is a large hexameric protein (molecular weight ~480,000 Da). It is composed of **six polypeptide chains**: 1. **Two Heavy Chains:** These wrap around each other in a double helix to form the "tail" (rod) of the molecule. At one end, they fold outward to form two globular "heads." 2. **Four Light Chains:** Two light chains are associated with each myosin head. These are categorized as **Essential Light Chains** (provide structural stability) and **Regulatory Light Chains** (regulate ATPase activity). **Analysis of Incorrect Options:** * **Option A (Two):** This refers only to the number of heavy chains. * **Option B (Four):** This refers only to the number of light chains. * **Option D (Eight):** This is incorrect as the standard Myosin II molecule does not contain eight subunits. **High-Yield Facts for NEET-PG:** * **The Myosin Head:** Contains two critical sites: the **Actin-binding site** and the **Catalytic site (ATP-binding site)** which has ATPase activity. * **HMM vs. LMM:** When treated with the enzyme trypsin, myosin breaks into **Heavy Meromyosin (HMM)**, which contains the heads and short neck (cross-bridges), and **Light Meromyosin (LMM)**, which forms the tail. * **Power Stroke:** The actual "rowing" motion occurs when ADP is released from the myosin head, causing it to tilt toward the arm. * **Clinical Correlation:** Mutations in the genes encoding cardiac myosin heavy chains are a primary cause of **Familial Hypertrophic Cardiomyopathy (HCM)**.

Q: Wallerian degeneration involves:

Successive fragmentation of the axon.. **Explanation:** **Wallerian Degeneration** refers to the sequence of events that occur distal to the site of a nerve injury (axotomy). [1] **1. Why Option C is Correct:** When an axon is severed, the distal segment loses its connection to the metabolic center (the cell body). Within 24–48 hours, the cytoskeleton breaks down, leading to the **successive fragmentation of the axon** and its myelin sheath. [1] This debris is subsequently cleared by macrophages and Schwann cells to prepare a path for potential regeneration. **2. Analysis of Incorrect Options:** * **Options A & D (Chromatolysis and Swelling of the cell body):** These describe the **Retrograde reaction** occurring in the *proximal* segment and the cell body (soma), not the distal segment. * **Option B (Only the CNS):** Wallerian degeneration occurs in both the Peripheral Nervous System (PNS) and the Central Nervous System (CNS). However, it is more efficient in the PNS due to Schwann cells; in the CNS, the process is slower and often inhibited by glial scarring. [2] **3. High-Yield Clinical Pearls for NEET-PG:** * **Timeline:** Degeneration begins within 24 hours; myelin sheath breakdown follows by day 3–5. * **Bands of Büngner:** These are columns of proliferating Schwann cells in the distal stump that guide the regenerating axon. [1] * **Nissl Substance:** Composed of Rough Endoplasmic Reticulum (RER); its disappearance (chromatolysis) is a hallmark of the cell body's response to injury. * **Regeneration Rate:** In the PNS, axons typically regrow at a rate of approximately **1–3 mm/day**.

Q: Which of the following statements is NOT true for smooth muscle?

The actin to myosin ratio is approximately 2:1.. ### Explanation **Why Option B is the Correct Answer (The False Statement):** In smooth muscle, the ratio of actin (thin filaments) to myosin (thick filaments) is significantly higher than in skeletal muscle. While skeletal muscle has a ratio of approximately 2:1 or 3:1, **smooth muscle has a ratio of about 10:1 to 15:1**. This high density of actin allows smooth muscle to generate significant force despite having less myosin. **Analysis of Other Options:** * **A. No Z-discs are present:** This is **true**. Smooth muscle lacks the organized sarcomere structure of striated muscle. Instead of Z-discs, thin filaments are anchored to **Dense Bodies** (composed of $\alpha$-actinin), which are distributed throughout the sarcoplasm and attached to the cell membrane. * **C. Contraction is primarily initiated by the thick filament:** This is **true**. Unlike skeletal muscle (thin-filament regulated via Troponin), smooth muscle is **thick-filament regulated**. Contraction begins when Calcium-Calmodulin activates **Myosin Light Chain Kinase (MLCK)**, which phosphorylates the myosin head. * **D. A 'latch bridge' phenomenon is observed:** This is **true**. This unique mechanism allows smooth muscle to maintain high tension for long periods with very low ATP consumption. It occurs when myosin is dephosphorylated while still attached to actin, slowing the detachment rate. **High-Yield NEET-PG Pearls:** * **Calmodulin** is the functional counterpart of Troponin C in smooth muscle. * **Troponin is absent** in smooth muscle; instead, **Caldesmon** and **Calponin** inhibit the actin-myosin interaction. * Smooth muscle can shorten to a much greater degree than skeletal muscle (up to 80% of its length). * **Caveolae** serve as rudimentary analogs to the T-tubule system.

Q: A 56-year-old woman with severe muscle weakness is hospitalized. The only abnormality in her laboratory values is an elevated serum K+ concentration. The elevated serum K+ causes muscle weakness because?

Na+ channels are closed by depolarization. ### Explanation **1. Why the Correct Answer is Right (Na+ channels are closed by depolarization)** In hyperkalemia, the increased extracellular $K^+$ concentration decreases the concentration gradient across the cell membrane. According to the **Nernst equation**, this causes the resting membrane potential (RMP) to become **less negative (depolarized)**. Initially, this brings the RMP closer to the threshold, making cells more excitable. However, **sustained depolarization** leads to the **inactivation of voltage-gated $Na^+$ channels**. These channels enter a "closed-and-not-ready" state (the inactivation gate or 'h' gate closes). Without functional $Na^+$ channels, the cell cannot generate an action potential, leading to muscle inexcitability and clinical weakness or paralysis. **2. Why the Other Options are Wrong** * **Option A:** The RMP is **depolarized** (becomes more positive), not hyperpolarized. Hyperpolarization would occur in hypokalemia. * **Option B:** The $K^+$ equilibrium potential ($E_K$) becomes **less negative** (e.g., moving from -90mV toward -70mV). This is a depolarizing shift, not hyperpolarization. * **Option C:** The $Na^+$ equilibrium potential is determined by $Na^+$ concentrations, which remain largely unaffected by changes in serum $K^+$. **3. Clinical Pearls for NEET-PG** * **ECG Changes in Hyperkalemia:** Tall peaked T-waves (earliest sign) $\rightarrow$ PR prolongation $\rightarrow$ Loss of P-wave $\rightarrow$ Widening of QRS (Sine wave pattern) $\rightarrow$ V-fib/Asystole. * **Management:** "C BIG K" (Calcium gluconate for membrane stabilization, Bicarbonate/Beta-agonists, Insulin + Glucose, Kayexalate/Dialysis). * **Membrane Stabilization:** Calcium gluconate does *not* lower $K^+$ levels; it antagonizes the membrane effects of hyperkalemia by shifting the threshold potential, restoring excitability.

Question 1

NN Nicotinic acetylcholine receptors are present on which of the following structures?

Accepted Answer

Presynaptic glutamate-secreting axon terminals

Answer

Myocardium

Answer

Motor endplates

Answer

Neuromuscular junction

Question 2

Which of the following is a true statement about smooth muscle?

Accepted Answer

Sarcomeres are absent in smooth muscle.

Answer

Smooth muscle cells have multiple nuclei.

Answer

Smooth muscle cells have striations.

Answer

Cross bridges are formed in smooth muscle during contraction.

Question 3

If the refractory period of a nerve is 1/2500th of a second, what is the maximum frequency of excitation of the nerve?

Accepted Answer

2500 times/sec

Answer

100 times/sec

Answer

250 times/sec

Answer

2000 times/sec

Question 4

Which of the following statements is NOT true regarding Type 1 muscle fibers?

Accepted Answer

High glycolytic capacity

Answer

High capillary density

Answer

High number of mitochondria

Answer

High myoglobin content

Question 5

Which of the following events happens when a nerve impulse arrives at the Neuromuscular Junction?

Accepted Answer

Acetylcholine binds to receptors on the postsynaptic sarcolemmal membrane

Answer

Release of Calcium from the Sarcoplasmic Reticulum

Answer

Efflux of calcium through synaptic vesicles into the synaptic cleft

Question 6

Each myosin molecule of a sarcomere is composed of how many monomers?

Accepted Answer

Six monomers

Answer

Two monomers

Answer

Four monomers

Answer

Eight monomers

Question 7

Wallerian degeneration involves:

Accepted Answer

Successive fragmentation of the axon.

Answer

Chromatolysis.

Answer

Only the central nervous system.

Answer

Swelling of the cell body.

Question 8

Which of the following statements is NOT true for smooth muscle?

Accepted Answer

The actin to myosin ratio is approximately 2:1.

Answer

No Z-discs are present.

Answer

Contraction is primarily initiated by the thick filament.

Answer

A 'latch bridge' phenomenon is observed.

Question 9

Arrange the following sequentially in the ascending order of occurrence with regard to signal transmission at the neuromuscular junction: Neurotransmitter degradation, Exocytosis, Calcium influx, End plate potential?

Accepted Answer

Calcium influx - Exocytosis - End plate potential - Neurotransmitter degradation

Answer

Neurotransmitter degradation - Exocytosis - Calcium influx - End plate potential

Answer

Calcium influx - Neurotransmitter degradation - Exocytosis - End plate potential

Answer

Exocytosis - End plate potential - Neurotransmitter degradation - Calcium influx

Question 10

A 56-year-old woman with severe muscle weakness is hospitalized. The only abnormality in her laboratory values is an elevated serum K+ concentration. The elevated serum K+ causes muscle weakness because?

Accepted Answer

Na+ channels are closed by depolarization

Answer

The resting membrane potential is hyperpolarized

Answer

The K+ equilibrium potential is hyperpolarized

Answer

The Na+ equilibrium potential is hyperpolarized

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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