Nerve and Muscle Physiology Practice Questions

Q: Calcium does not bind to

Tropomyosin. ***Tropomyosin*** - **Tropomyosin** is a protein that winds around **actin filaments** and, in relaxed muscle, blocks the **myosin-binding sites** on actin, preventing contraction. - Calcium does **not directly bind** to tropomyosin; rather, its binding to **troponin** causes a conformational change that moves tropomyosin away from the binding sites. - **This is the correct answer** because tropomyosin lacks calcium-binding sites. *Incorrect: Troponin* - **Troponin** is a complex of three proteins (**troponin I, T, and C**) that is crucial for muscle contraction. - **Troponin C** is the specific subunit that **binds calcium ions**, initiating the cascade of events leading to muscle contraction. - This option is incorrect because troponin DOES bind calcium. *Incorrect: Calmodulin* - **Calmodulin** is a ubiquitous **calcium-binding messenger protein** expressed in all eukaryotic cells. - It mediates many crucial cellular processes by interacting with and regulating various protein targets (e.g., kinases, phosphatases) when it **binds to calcium ions**. - This option is incorrect because calmodulin DOES bind calcium. *Incorrect: None of the options* - This option would suggest that all the listed proteins bind calcium. - Since **tropomyosin does NOT bind calcium**, this option is incorrect.

Q: A pole vaulter had a fall during pole vaulting and had paralysis of the arm . Which of the following investigations gives the best recovery prognosis -

Electromyography. Electromyography - **Electromyography (EMG)** can help assess the extent of nerve damage and reinnervation, providing insights into the potential for recovery [1]. - The presence of **spontaneous activity** (fibrillations, positive sharp waves) indicates denervation, while the appearance of **motor unit action potentials (MUAPs)** suggests reinnervation [1]. *Creatine phosphokinase levels* - **Creatine phosphokinase (CPK)** levels primarily indicate **muscle damage**, not the extent of nerve injury or recovery potential. - While muscle damage can occur with nerve injury, CPK does not provide specific prognostic information for nerve regeneration. *Strength Duration Curve* - The **strength duration curve** assesses the excitability of a nerve or muscle to electrical stimulation. - While it can differentiate between **nerve and muscle damage**, it provides less comprehensive prognostic information compared to EMG regarding the status of nerve regeneration. *Muscle biopsy* - A **muscle biopsy** would directly evaluate muscle pathology, such as atrophy or regeneration. - However, it is an **invasive procedure** and provides less direct information about nerve recovery compared to EMG, which directly assesses nerve and muscle electrical activity.

Q: Demyelination is the major feature of Multiple Sclerosis. Which of the following cells forms myelin in the central nervous system?

Oligodendrocytes. ***Oligodendrocytes*** - **Oligodendrocytes** are glial cells exclusively found in the **central nervous system (CNS)** that produce and maintain the **myelin sheath**. - The myelin sheath, formed by these cells, insulates axons and allows for rapid, efficient **saltatory conduction** of action potentials. *Astrocytes* - **Astrocytes** are star-shaped glial cells that provide structural and metabolic support for neurons, regulate the **blood-brain barrier**, and maintain the extracellular environment. - They do not form myelin; instead, they play roles in **neurotransmission** and response to injury. *Ependymal cells* - **Ependymal cells** line the ventricles of the brain and the central canal of the spinal cord, forming an interface between the neural tissue and **cerebrospinal fluid (CSF)**. - They are involved in **CSF production** and circulation, having no role in myelination. *Microglia* - **Microglia** are the resident immune cells of the CNS, functioning as **macrophages** to remove cellular debris, pathogens, and damaged neurons. - They are crucial for immune surveillance and inflammatory responses but do not produce myelin.

Q: The protein responsible for elasticity of the muscle is:

Titin. ***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.

Q: The Nernst potential of K+ is (in mV):

-90. ***-90*** - The **Nernst potential** for K+ is approximately -90 mV, the standard textbook value used in medical education, calculated using the Nernst equation with typical intracellular (140 mEq/L) and extracellular (4 mEq/L) concentrations of K+. - This value represents the **equilibrium potential** at which there is no net movement of potassium ions across the cell membrane. - This rounded value is consistently cited in standard physiology texts (Ganong, Guyton) and is the expected answer for medical examinations. *-10* - This value is significantly less negative than the actual Nernst potential for K+ and does not reflect the typical concentration gradient of potassium. - An equilibrium potential of -10 mV would imply a much smaller concentration gradient or a different ion species. *-61* - This value is close to the typical **resting membrane potential** of many excitable cells (around -70 mV), but not the Nernst potential for K+ specifically. - The resting membrane potential is a weighted average of the Nernst potentials of several ions, with K+ being a major contributor due to its high permeability. *-94* - While this represents a more precise calculation using the Nernst equation, **-90 mV is the standard textbook value** taught in medical physiology and expected in examinations. - The difference between -90 and -94 mV reflects rounding conventions; -90 mV is universally accepted in clinical and academic contexts.

Q: Find the true statement regarding sensory endings

Flower spray is secondary. ***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.

Q: Golgi tendon organ function is?

Detects the muscle tension. ***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.

Q: Absolute refractoriness of a neuron is due to?

Inactivation of Na channels. ***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.

Q: Acetylcholine release can be increased from presynaptic membrane by:

Blocking voltage gated K+ channels on presynaptic membrane. ***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.

Q: What is the role of myelin in the nervous system?

Increase conduction speed. ***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 1

Calcium does not bind to

Accepted Answer

Tropomyosin

Answer

Troponin

Answer

Calmodulin

Answer

None of the options

Question 2

A pole vaulter had a fall during pole vaulting and had paralysis of the arm . Which of the following investigations gives the best recovery prognosis -

Accepted Answer

Electromyography

Answer

Strength Duration Curve

Answer

Creatine phosphokinase levels

Answer

Muscle biopsy

Question 3

Demyelination is the major feature of Multiple Sclerosis. Which of the following cells forms myelin in the central nervous system?

Accepted Answer

Oligodendrocytes

Answer

Astrocytes

Answer

Ependymal cells

Answer

Microglia

Question 4

The protein responsible for elasticity of the muscle is:

Accepted Answer

Titin

Answer

Myosin

Answer

Actin

Answer

Tropomyosin

Question 5

The Nernst potential of K+ is (in mV):

Accepted Answer

-90

Answer

-10

Answer

-61

Answer

-94

Question 6

Find the true statement regarding sensory endings

Accepted Answer

Flower spray is secondary

Answer

Annulospiral wrap the ends

Answer

Primary ending is flower spray

Answer

Primary ending conduct 1b fibres

Question 7

Golgi tendon organ function is?

Accepted Answer

Detects the muscle tension

Answer

Detects the dynamic change in muscle length

Answer

Detects the muscle stretch

Answer

Detects the muscle strength

Question 8

Absolute refractoriness of a neuron is due to?

Accepted Answer

Inactivation of Na channels

Answer

Hyperpolarization of Cl channels

Answer

Opening of rectifier K+ channels

Answer

Closure of activated Na channels

Question 9

Acetylcholine release can be increased from presynaptic membrane by:

Accepted Answer

Blocking voltage gated K+ channels on presynaptic membrane

Answer

Blocking voltage gated Cl- channels on presynaptic membrane

Answer

Blocking voltage gated Na+ channels on presynaptic membrane

Answer

Blocking voltage gated Ca2+ channels on presynaptic membrane

Question 10

What is the role of myelin in the nervous system?

Accepted Answer

Increase conduction speed

Answer

Increase synaptic delay

Answer

Increase capacitance

Answer

Decrease electrical resistance

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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