Nerve and Muscle Physiology Practice Questions

Q: Which of the following is an anchoring protein?

Actinin. **Explanation:** The correct answer is **Actinin**. **1. Why Actinin is the Correct Answer:** Anchoring proteins (also known as linking or scaffolding proteins) are responsible for tethering the cytoskeleton to specific structures within the cell. **$\alpha$-Actinin** is a major cross-linking protein found in the **Z-disk** of skeletal muscle. Its primary function is to anchor the ends of the thin (actin) filaments to the Z-disk, ensuring the structural stability of the sarcomere during muscle contraction. **2. Analysis of Incorrect Options:** * **Myosin (Option A):** This is a **contractile protein**. It forms the thick filaments and possesses ATPase activity to generate force via the sliding filament mechanism. * **Troponin (Option C):** This is a **regulatory protein** complex (consisting of subunits T, I, and C). It binds calcium and moves tropomyosin to uncover myosin-binding sites on actin. * **Tropomyosin (Option D):** This is also a **regulatory protein**. It winds around the actin helix and blocks the active sites in a resting muscle to prevent contraction. **3. NEET-PG High-Yield Clinical Pearls:** * **Dystrophin:** Another critical anchoring protein. It links the actin cytoskeleton to the extracellular matrix. Mutations in the *DMD* gene lead to **Duchenne Muscular Dystrophy**. * **Titin:** The largest known protein; it acts as a molecular spring, anchoring the thick (myosin) filaments to the Z-disk and providing passive elasticity. * **Desmin:** An intermediate filament that anchors Z-disks of adjacent myofibrils to each other and to the plasma membrane (sarcolemma). * **Z-Disk Composition:** Remember that the Z-disk marks the boundary of a sarcomere and contains $\alpha$-actinin, desmin, and vimentin.

Q: What is true about neuropraxia?

Physiological block. **Explanation:** **Neuropraxia** is the mildest form of nerve injury according to **Seddon’s classification**. It is characterized by a **physiological block** of nerve conduction without any structural damage to the axon or the connective tissue sheaths (epineurium, perineurium, and endoneurium). 1. **Why the correct answer is right:** In neuropraxia, the nerve remains anatomically intact, but conduction is temporarily halted, usually due to focal demyelination or ischemia caused by sustained pressure (e.g., Saturday Night Palsy). Since the axon is preserved, there is **no Wallerian degeneration** distal to the site of injury. Recovery is typically spontaneous and complete within days to weeks once the pressure is relieved. 2. **Why the incorrect options are wrong:** * **Blockage of axon:** This is misleading. While conduction is blocked, the physical continuity of the axon is not interrupted. * **Incomplete/Complete transection:** These describe higher grades of injury. **Axonotmesis** involves axonal disruption with preservation of the sheath, while **Neurotmesis** (Option D) involves complete transection of both the axon and the connective tissue, requiring surgical intervention. **High-Yield Facts for NEET-PG:** * **Seddon’s Classification:** Neuropraxia (Mildest) → Axonotmesis → Neurotmesis (Most severe). * **Sunderland’s Classification:** Neuropraxia corresponds to **First-degree** injury. * **Clinical Feature:** Motor fibers are more susceptible than sensory fibers; autonomic functions are usually preserved. * **EMG Finding:** No denervation potentials (fibrillations) are seen because the axon is intact.

Q: During the repolarization phase of the action potential of a neuron, which of the following occurs?

Increased permeability to K+ ion. **Explanation:** The action potential is a rapid change in membrane potential characterized by sequential changes in ion permeability. **Repolarization** is the phase where the membrane potential returns toward the resting level after peak depolarization. **Why Option A is Correct:** Repolarization is primarily driven by two simultaneous events: 1. **Inactivation of Voltage-Gated Na+ Channels:** The "h-gates" (inactivation gates) close, stopping the influx of sodium. 2. **Activation of Voltage-Gated K+ Channels:** These channels open (though more slowly than Na+ channels), leading to a marked **increase in K+ permeability**. Since the concentration of K+ is higher inside the cell, K+ ions exit the cell (efflux), carrying positive charges out and restoring the negative resting membrane potential. **Why Other Options are Incorrect:** * **Option B:** Decreased K+ permeability would prevent the cell from returning to its resting state, leading to prolonged depolarization. * **Option C:** Increased Ca2+ permeability is characteristic of the **plateau phase** in cardiac muscle action potentials, not the standard neuronal repolarization. * **Option D:** Increased Na+ permeability is the hallmark of the **Depolarization phase**. **High-Yield NEET-PG Pearls:** * **Hyperpolarization:** Occurs because K+ channels are slow to close, allowing the membrane potential to become more negative than the resting membrane potential (RMP). * **Absolute Refractory Period:** Corresponds to the period from the threshold to the early part of repolarization (due to Na+ channel inactivation). * **Tetraethylammonium (TEA):** A pharmacological tool that blocks voltage-gated K+ channels, thereby abolishing the repolarization phase.

Q: After the application of a stimulus, a change in neuronal membrane potential occurs without the opening of gated ion channels. What is this change in membrane potential called?

Electrotonic potential. ### Explanation The correct answer is **Electrotonic potential**. **1. Why Electrotonic Potential is Correct:** Electrotonic potentials (also known as passive potentials) are non-propagated local changes in membrane potential that occur due to the **passive physical properties** of the cell membrane. Unlike action potentials or graded local potentials, they do **not** involve the opening or closing of voltage-gated or ligand-gated ion channels. Instead, they result from the direct spread of electrical current through the membrane’s capacitance and resistance. These potentials are characterized by being **decremental** (fading with distance) and **graded** (proportional to stimulus intensity). **2. Why the Other Options are Incorrect:** * **Action Potential:** This is an "all-or-none" phenomenon that **requires** the opening of voltage-gated sodium and potassium channels once the threshold is reached. * **Local Potential (Graded Potential):** While similar to electrotonic potentials in being localized, local potentials (like EPSPs or receptor potentials) typically involve the opening of **ligand-gated or mechanical ion channels**. * **Resting Potential:** This is the static membrane potential (usually -70mV to -90mV) maintained when the neuron is not being stimulated, primarily by K+ leak channels and the Na+/K+ ATPase pump. **3. High-Yield NEET-PG Pearls:** * **Length Constant ($\lambda$):** The distance at which an electrotonic potential falls to 37% of its original value. Higher membrane resistance and lower internal resistance increase the length constant. * **Time Constant ($\tau$):** The time taken for the potential to reach 63% of its final value. * **Clinical Significance:** Electrotonic spread is crucial for **summation** (temporal and spatial) at the axon hillock. In myelinated neurons, the current spreads electrotonically between the Nodes of Ranvier (Saltatory conduction).

Q: The inverse stretch reflex is mediated by which of the following structures?

Golgi tendon organ. **Explanation:** The **Inverse Stretch Reflex** (also known as the autogenic inhibition reflex) is a protective mechanism that prevents muscle damage due to excessive tension. **1. Why Golgi Tendon Organ (GTO) is correct:** The GTO is the sensory receptor for this reflex, located at the junction of muscle fibers and tendons. Unlike the muscle spindle, which responds to changes in muscle *length*, the GTO is arranged in **series** with muscle fibers and responds primarily to **muscle tension** (force). When a muscle undergoes heavy contraction, the GTO is stimulated and sends impulses via **Type Ib afferent fibers** to the spinal cord. These fibers synapse on inhibitory interneurons, which then inhibit the alpha motor neurons of the same muscle, causing it to relax. **2. Why other options are incorrect:** * **Muscle Spindle:** This is the receptor for the **Stretch Reflex** (Myotatic reflex). It is arranged in **parallel** with extrafusal fibers and responds to changes in muscle **length**. * **Trail and Tail fibre endings:** These terms refer to the types of motor nerve endings on intrafusal muscle fibers. **Trail endings** are typically found on nuclear chain fibers, while **Plate endings** (often confused with "tail") are on nuclear bag fibers. They are involved in the efferent (motor) gamma system, not the afferent limb of the inverse stretch reflex. **Clinical Pearls for NEET-PG:** * **Receptor:** Golgi Tendon Organ (Tension sensor). * **Afferent Nerve:** Type Ib (Fast conducting). * **Synapse:** Polysynaptic (involves an inhibitory interneuron). * **Function:** Prevents tendon avulsion and muscle tearing during extreme exertion. * **Clasp-knife response:** In upper motor neuron (UMN) lesions, the sudden relaxation of a spastic muscle upon passive stretching is attributed to the activation of the inverse stretch reflex.

Q: Which of the following are supportive proteins?

All of the above. In the context of muscle neuroanatomy and physiology, **supportive proteins** (also known as cytoskeletal or structural proteins) are essential for maintaining the architectural integrity, alignment, and elastic properties of the muscle fiber during contraction and relaxation. [1] **Explanation of the Correct Answer:** The correct answer is **All of the above** because each of these proteins plays a specific structural role in the sarcomere or the muscle fiber: * **Desmin (Option A):** This is an intermediate filament protein that links adjacent myofibrils at the Z-discs. [2] It ensures that all myofibrils within a muscle fiber contract in unison and anchors them to the sarcolemma. * **Dystrophin (Option B):** This is a vital subsarcolemmal protein that connects the internal cytoskeleton (actin) to the extracellular matrix via the dystroglycan complex. It acts as a "shock absorber," protecting the sarcolemma from mechanical stress during contraction. [1] * **Titin (Option C):** Known as the largest protein in the human body, Titin acts as a molecular spring. It extends from the Z-disc to the M-line, centering the myosin (thick) filaments and providing passive elasticity to the muscle. [2] **Clinical Pearls for NEET-PG:** * **Duchenne Muscular Dystrophy (DMD):** Caused by an X-linked recessive mutation leading to a complete absence of **Dystrophin**, resulting in progressive muscle fiber necrosis. [1] * **Becker Muscular Dystrophy:** Involves a truncated or partially functional form of Dystrophin. * **Titin Mutations:** Often associated with Dilated Cardiomyopathy (DCM). * **Nebulin:** Another high-yield supportive protein that acts as a "ruler" to regulate the length of actin (thin) filaments.

Q: The resting membrane potential (RMP) of a nerve cell is equal to the equilibrium potential of which ion?

Cl-. **Explanation:** The Resting Membrane Potential (RMP) of a cell is determined by the permeability of the membrane to specific ions and their respective concentration gradients. **Why Cl- is the Correct Answer:** In many neurons, chloride ions ($Cl^-$) are **passively distributed** across the cell membrane. This means there is no active transport mechanism (like a pump) moving chloride against its gradient. Consequently, $Cl^-$ shifts across the membrane until it reaches an equilibrium where the electrical gradient perfectly balances the chemical gradient. Therefore, the equilibrium potential ($E_{Cl}$) often aligns exactly with the RMP (typically -70 mV to -90 mV). **Analysis of Incorrect Options:** * **K+ (Potassium):** While the RMP is *closest* to the equilibrium potential of $K^+$ (approx. -94 mV) because the membrane is highly permeable to it, they are not equal. The slight influx of $Na^+$ prevents the RMP from reaching the full $E_K$. * **Na+ (Sodium):** The equilibrium potential for $Na^+$ is positive (approx. +60 mV). At rest, the membrane has very low permeability to $Na^+$, so the RMP stays far from this value. * **Ca2+ (Calcium):** Similar to sodium, $Ca^{2+}$ has a positive equilibrium potential and very low resting permeability; it does not determine the RMP. **High-Yield Clinical Pearls for NEET-PG:** * **Goldman-Hodgkin-Katz Equation:** This equation calculates the RMP by considering the permeability and concentration of all major ions ($Na^+$, $K^+$, $Cl^-$). * **Nernst Equation:** Used to calculate the equilibrium potential for a *single* ion. * **The Na+-K+ ATPase Pump:** This is "electrogenic" and contributes about -5 to -10 mV directly to the RMP, but its primary role is maintaining the concentration gradients that allow the RMP to exist. * **Key Concept:** If an ion is distributed purely passively, its equilibrium potential **must** equal the RMP.

Q: Maximum number of Na+ channels per square micrometer is present in which of the following locations?

Nodes of Ranvier. ### Explanation The density of voltage-gated sodium (Na+) channels is the primary determinant of the threshold for excitation and the velocity of impulse conduction. **Why Nodes of Ranvier is correct:** In myelinated neurons, the **Nodes of Ranvier** contain the highest concentration of voltage-gated Na+ channels, estimated at **2,000 to 12,000 per μm²**. This extreme density is essential for **saltatory conduction**, allowing the action potential to "jump" from node to node. This mechanism ensures rapid signal transmission while conserving energy, as depolarization is restricted to these small gaps rather than the entire axonal membrane. **Why the other options are incorrect:** * **Cell body (Soma):** The density here is relatively low (approx. 50–75 per μm²), as the soma is primarily involved in metabolic functions rather than rapid signal propagation. * **Axon terminal:** While it contains Na+ channels, the terminal is more densely packed with voltage-gated **calcium (Ca²+) channels** to facilitate neurotransmitter release. * **Surface of myelin:** Myelin acts as an insulator. The axonal membrane underneath the myelin sheath is nearly devoid of Na+ channels; instead, it contains potassium (K+) channels in the juxtaparanodal regions. **High-Yield Clinical Pearls for NEET-PG:** * **Axon Hillock:** This is the site where the action potential is typically **initiated** because it has the lowest threshold for excitation (density ~350–500 per μm²). * **Demyelinating Diseases:** In conditions like **Multiple Sclerosis**, the loss of myelin exposes the internodal membrane (which lacks Na+ channels), leading to conduction block or slowing. * **Unmyelinated Axons:** The Na+ channel density is uniform but low (approx. 110 per μm²) compared to the Nodes of Ranvier.

Question 1

Which of the following is an anchoring protein?

Accepted Answer

Actinin

Answer

Myosin

Answer

Troponin

Answer

Tropomyosin

Question 2

Repolarization of a nerve action potential is due to which of the following?

Accepted Answer

Outward potassium current and inward sodium current

Answer

Inward sodium current

Answer

Inward potassium current

Answer

Inward potassium current and outward sodium current

Question 3

What is true about neuropraxia?

Accepted Answer

Physiological block

Answer

Blockage of axon

Answer

Incomplete transection of nerve

Answer

Complete transection of nerve

Question 4

During the repolarization phase of the action potential of a neuron, which of the following occurs?

Accepted Answer

Increased permeability to K+ ion

Answer

Decreased permeability to K+ ion

Answer

Increased permeability to Ca2+ ion

Answer

Increased permeability to Na+ ion

Question 5

After the application of a stimulus, a change in neuronal membrane potential occurs without the opening of gated ion channels. What is this change in membrane potential called?

Accepted Answer

Electrotonic potential

Answer

Action potential

Answer

Local potential

Answer

Resting potential

Question 6

What is the predominant determinant of the amplitude of the action potential?

Accepted Answer

Equilibrium potential of Cl-

Answer

Equilibrium potential of Na+

Answer

Equilibrium potential of K+

Answer

Equilibrium potential of HCO3-

Question 7

The inverse stretch reflex is mediated by which of the following structures?

Accepted Answer

Golgi tendon organ

Answer

Trail fibre ending

Answer

Tail fibre ending

Answer

Muscle spindle

Question 8

Which of the following are supportive proteins?

Accepted Answer

All of the above

Answer

Desmin

Answer

Dystrophin

Answer

Titin

Question 9

The resting membrane potential (RMP) of a nerve cell is equal to the equilibrium potential of which ion?

Accepted Answer

Cl-

Answer

K+

Answer

Na+

Answer

Ca+

Question 10

Maximum number of Na+ channels per square micrometer is present in which of the following locations?

Accepted Answer

Nodes of Ranvier

Answer

Cell body

Answer

Axon terminal

Answer

Surface of myelin

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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