Chapter: Physiology; Topic: Thermoregulation; Subtopic: Mechanism of Fever
Keyword Definitions:
• Endogenous Pyrogens: Cytokines like IL-1, IL-6, and TNF-α produced by immune cells that mediate fever.
• Hypothalamic Set Point: Temperature level regulated by the preoptic area of the hypothalamus.
• PGE2: Prostaglandin E2, a lipid mediator that raises hypothalamic temperature set point during fever.
• Thermoregulation: Physiological process maintaining internal temperature through heat production and loss mechanisms.
Lead Question - 2014
Endogenous pyrogens act by ?
a) Increasing heat generation
b) Raising thermostat point of hypothalamus
c) Causing vasoconstriction
d) By Non-shivering thermogenesis
Answer & Explanation: Correct answer is b) Raising thermostat point of hypothalamus. Endogenous pyrogens such as IL-1, IL-6, and TNF-α trigger the synthesis of PGE2 in the hypothalamic preoptic area, elevating the temperature set point. The body perceives its normal temperature as low and activates heat-generating mechanisms like shivering and vasoconstriction to raise temperature. This process continues until the body temperature reaches the new set point, resulting in fever. This mechanism aids immune function by inhibiting microbial growth. When pyrogenic signals subside, antipyretic mechanisms like sweating and vasodilation restore normal temperature.
1) Which cytokine is the most potent endogenous pyrogen?
a) IL-1
b) IL-10
c) Interferon-gamma
d) TNF-beta
Answer & Explanation: Correct answer is a) IL-1. IL-1 is a major endogenous pyrogen released by macrophages. It stimulates hypothalamic PGE2 production, elevating the set point for temperature regulation, thereby initiating the febrile response.
2) Fever differs from hyperthermia because:
a) Both are caused by external heat
b) Set-point increases in fever
c) Set-point decreases in fever
d) Fever has no hypothalamic control
Answer & Explanation: Correct answer is b) Set-point increases in fever. In fever, hypothalamic set-point rises due to PGE2, while in hyperthermia, body temperature rises above the set-point due to external or metabolic causes without hypothalamic involvement.
3) The main site of PGE2 synthesis during fever is:
a) Hippocampus
b) Preoptic area of hypothalamus
c) Cerebellum
d) Medulla oblongata
Answer & Explanation: Correct answer is b) Preoptic area of hypothalamus. PGE2 acts here to elevate the set-point temperature, resulting in activation of heat conservation and production mechanisms that induce fever.
4) During fever, the body initiates heat conservation by:
a) Vasodilation
b) Vasoconstriction
c) Perspiration
d) Sweating
Answer & Explanation: Correct answer is b) Vasoconstriction. To conserve heat, cutaneous vessels constrict, reducing blood flow to skin and minimizing heat loss, which helps elevate core temperature to the new hypothalamic set-point.
5) Exogenous pyrogens cause fever by:
a) Directly raising hypothalamic set-point
b) Stimulating endogenous cytokine release
c) Activating sweat glands
d) Inhibiting IL-6 production
Answer & Explanation: Correct answer is b) Stimulating endogenous cytokine release. Exogenous pyrogens like bacterial lipopolysaccharides induce immune cells to produce IL-1 and TNF-α, which in turn raise the hypothalamic set-point through PGE2 synthesis.
6) A patient with infection develops chills before fever. The chills are due to:
a) Decreased body temperature
b) Set-point rising above body temperature
c) Sweating
d) Vasodilation
Answer & Explanation: Correct answer is b) Set-point rising above body temperature. The hypothalamus perceives current temperature as low and activates shivering and vasoconstriction to generate heat, causing chills before the actual rise in temperature.
7) Which of the following is not an endogenous pyrogen?
a) IL-6
b) TNF-α
c) IL-10
d) IL-1
Answer & Explanation: Correct answer is c) IL-10. IL-10 is an anti-inflammatory cytokine that suppresses immune activation and downregulates proinflammatory mediators, thereby reducing fever and inflammation.
8) Which antipyretic drug inhibits prostaglandin synthesis?
a) Paracetamol
b) Atropine
c) Dopamine
d) Epinephrine
Answer & Explanation: Correct answer is a) Paracetamol. Paracetamol (acetaminophen) inhibits cyclooxygenase enzymes in the CNS, thereby reducing PGE2 synthesis in the hypothalamus and lowering the elevated set-point temperature.
9) Which organ detects and controls body temperature changes?
a) Hypothalamus
b) Thalamus
c) Medulla
d) Pituitary gland
Answer & Explanation: Correct answer is a) Hypothalamus. The hypothalamus integrates signals from thermoreceptors and controls autonomic responses to maintain body temperature within physiological limits during fever or cold exposure.
10) Clinical case: A 45-year-old male develops fever after bacterial infection. The fever subsides after taking ibuprofen. What is the mechanism?
a) Increased vasoconstriction
b) Inhibition of PGE2 synthesis
c) Decreased IL-6 secretion
d) Activation of sweat glands
Answer & Explanation: Correct answer is b) Inhibition of PGE2 synthesis. Ibuprofen inhibits COX enzymes, reducing PGE2 production in the hypothalamus, thereby lowering the elevated temperature set-point and promoting heat loss through sweating and vasodilation.
Chapter: Physiology; Topic: Hypothalamic Regulation of Appetite; Subtopic: Neuroendocrine Control of Feeding Behavior
Keyword Definitions:
Appetite: Desire for food regulated by hypothalamic centers, influenced by hormones and neurotransmitters.
Arcuate nucleus: A hypothalamic region that contains neurons regulating hunger and satiety.
NPY (Neuropeptide Y): A potent appetite stimulant found in the hypothalamus.
AGRP (Agouti-related peptide): A neuropeptide that increases food intake by antagonizing melanocortin receptors.
CART (Cocaine- and amphetamine-regulated transcript): A peptide that suppresses appetite.
α-MSH (Alpha-melanocyte-stimulating hormone): A peptide that decreases appetite via MC4 receptors.
Insulin: Hormone that decreases appetite by acting on hypothalamic centers.
Lead Question – 2014
Which of the following increases appetite?
a) CART
b) α - MSH
c) AGPP
d) Insulin
Explanation: The correct answer is AGRP (Agouti-related peptide). AGRP stimulates appetite by inhibiting melanocortin receptors (MC3 and MC4) in the hypothalamus, promoting feeding behavior. It acts synergistically with Neuropeptide Y, both secreted from arcuate nucleus neurons. CART and α-MSH suppress appetite, while insulin also inhibits food intake via satiety signaling pathways.
1) Which hormone secreted from the stomach stimulates appetite?
a) Ghrelin
b) Leptin
c) Insulin
d) CCK
Explanation: The answer is Ghrelin. It is a peptide hormone produced by the stomach that increases appetite by acting on hypothalamic neurons, especially the NPY/AGRP group. Ghrelin levels rise before meals and fall afterward, signaling hunger to maintain energy balance through hypothalamic stimulation of feeding behavior.
2) Which center of the hypothalamus is known as the hunger center?
a) Ventromedial nucleus
b) Lateral hypothalamic area
c) Arcuate nucleus
d) Paraventricular nucleus
Explanation: The correct answer is Lateral hypothalamic area. It contains neurons that stimulate feeding when activated. Damage to this region leads to anorexia. It integrates peripheral signals like ghrelin and glucose levels, modulating neuronal activity to promote hunger sensations and maintain energy homeostasis in the body.
3) Which hypothalamic nucleus acts as the satiety center?
a) Lateral hypothalamus
b) Ventromedial nucleus
c) Arcuate nucleus
d) Posterior hypothalamus
Explanation: The correct answer is Ventromedial nucleus. It inhibits feeding behavior when stimulated. Lesions in this area cause hyperphagia and obesity. It receives leptin and insulin signals, reducing food intake by suppressing hunger-promoting neurons in the lateral hypothalamus and maintaining energy balance.
4) Which neurotransmitter promotes satiety and reduces appetite?
a) Dopamine
b) Serotonin
c) Norepinephrine
d) Glutamate
Explanation: The correct answer is Serotonin. It acts on hypothalamic receptors to reduce appetite and food intake, particularly carbohydrates. Serotonin increases satiety through activation of POMC neurons and inhibition of NPY/AGRP neurons. Drugs enhancing serotonin activity can help reduce appetite and support weight management.
5) Which of the following is an anorexigenic hormone?
a) Ghrelin
b) Neuropeptide Y
c) Leptin
d) AGRP
Explanation: The correct answer is Leptin. Secreted by adipose tissue, it signals energy sufficiency to the hypothalamus, reducing appetite. It inhibits NPY and AGRP neurons while stimulating POMC/CART neurons, promoting satiety. Leptin deficiency or resistance is associated with obesity and altered energy homeostasis in humans.
6) A 45-year-old obese patient shows leptin resistance. Which mechanism explains his persistent hunger?
a) Increased CART activity
b) Impaired hypothalamic leptin signaling
c) Enhanced α-MSH sensitivity
d) Decreased ghrelin secretion
Explanation: The answer is Impaired hypothalamic leptin signaling. Leptin resistance prevents satiety signaling, causing continued food intake despite energy sufficiency. It leads to altered neuronal responses in the arcuate nucleus, persistent hunger, and weight gain due to failure of leptin-mediated appetite suppression mechanisms.
7) A person deprived of sleep for several days reports increased hunger. Which hormone likely increased?
a) Leptin
b) Ghrelin
c) Insulin
d) CART
Explanation: The answer is Ghrelin. Sleep deprivation increases ghrelin and decreases leptin, stimulating appetite and preference for high-calorie foods. This imbalance promotes weight gain. Ghrelin acts on hypothalamic centers, enhancing NPY and AGRP activity, which trigger hunger signals during energy deficit or sleep loss.
8) Which hypothalamic peptide increases appetite during fasting?
a) CART
b) AGRP
c) CRH
d) Somatostatin
Explanation: The correct answer is AGRP. Fasting increases AGRP expression in arcuate neurons, stimulating appetite. AGRP inhibits melanocortin receptors that normally suppress feeding. This compensatory mechanism helps restore energy balance during caloric restriction or prolonged fasting conditions.
9) A patient with hypothalamic tumor affecting the lateral hypothalamus presents with weight loss and loss of appetite. What is the likely mechanism?
a) Overactivation of AGRP neurons
b) Damage to hunger center
c) Hyperleptinemia
d) Ghrelin excess
Explanation: The answer is Damage to hunger center. The lateral hypothalamus is responsible for stimulating appetite. Tumor-induced damage leads to anorexia, weight loss, and decreased feeding behavior, demonstrating its critical role in energy intake regulation.
10) A child presents with hyperphagia and obesity due to a mutation in the leptin receptor gene. What happens to appetite control?
a) Increased leptin sensitivity
b) Impaired satiety signaling
c) Reduced ghrelin secretion
d) Enhanced α-MSH response
Explanation: The correct answer is Impaired satiety signaling. Mutation in leptin receptor prevents leptin from inhibiting appetite-regulating neurons in the hypothalamus, leading to uncontrolled hunger, hyperphagia, and early-onset obesity despite high leptin levels in circulation.
Chapter: Physiology Topic: Nervous System; Subtopic: Pain Pathways and Nerve Fiber Types
Keyword Definitions:
Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
Nociceptors: Specialized sensory receptors that detect damaging or potentially damaging stimuli.
Aδ fibers: Thinly myelinated fibers transmitting sharp, localized “first pain.”
C fibers: Unmyelinated fibers transmitting dull, burning “second pain.”
Myelination: Fatty insulation of axons increasing conduction velocity.
Dorsal horn: Region in spinal cord receiving sensory input from nociceptors.
Spinothalamic tract: Major ascending pathway conveying pain and temperature sensations to the brain.
Lead Question – 2014
Sharp pain is transmitted by which type of fibres?
a) Aα
b) Aβ
c) Aδ
d) C
Explanation: The correct answer is Aδ fibers. These are thinly myelinated nerve fibers that transmit sharp, localized, and fast pain sensations. They conduct impulses at a velocity of 5–30 m/s. The pain they mediate is often called “first pain.” In contrast, unmyelinated C fibers transmit dull, burning, and poorly localized “second pain” at slower speeds.
1) Which fibers transmit slow, burning pain?
a) Aα
b) Aβ
c) Aδ
d) C
Explanation: The correct answer is C fibers. These are unmyelinated, small-diameter fibers that conduct impulses at 0.4–2 m/s. They carry dull, throbbing, and persistent pain known as “second pain.” Their slow conduction allows prolonged perception of tissue injury and contributes to protective behavior and healing awareness.
2) Which part of the brain perceives pain intensity and localization?
a) Thalamus
b) Cerebellum
c) Hypothalamus
d) Hippocampus
Explanation: The correct answer is Thalamus. The thalamus acts as a relay center for sensory impulses, including pain, directing them to the somatosensory cortex. It helps localize and interpret pain intensity before emotional components are processed in the limbic system.
3) Which neurotransmitter is primarily involved in transmission of pain in the spinal cord?
a) Dopamine
b) Glutamate
c) Acetylcholine
d) GABA
Explanation: The correct answer is Glutamate. It is the main excitatory neurotransmitter in nociceptive pathways, particularly in Aδ fiber synapses within the dorsal horn. Substance P is also involved, particularly in chronic pain transmission via C fibers and secondary sensory neurons.
4) Which fibers are responsible for tactile sensations like touch and pressure?
a) Aα
b) Aβ
c) Aδ
d) C
Explanation: The correct answer is Aβ fibers. These are large, heavily myelinated fibers that conduct sensory impulses rapidly. They are primarily responsible for transmitting non-noxious stimuli like touch, pressure, and vibration, helping differentiate pain from normal tactile sensations.
5) Which tract transmits pain and temperature sensations to the brain?
a) Dorsal column
b) Corticospinal tract
c) Spinothalamic tract
d) Vestibulospinal tract
Explanation: The correct answer is Spinothalamic tract. This ascending pathway originates in the dorsal horn of the spinal cord and carries pain and temperature sensations to the thalamus and somatosensory cortex, enabling conscious pain perception and localization.
6) A patient reports sharp pain immediately after a needle prick. Which fibers are involved?
a) Aδ fibers
b) C fibers
c) Aβ fibers
d) B fibers
Explanation: The correct answer is Aδ fibers. These fibers rapidly transmit the initial sharp pain from mechanical or thermal stimuli. Their conduction speed allows quick withdrawal reflexes, helping prevent further tissue damage before slow C fiber pain begins.
7) A patient with peripheral neuropathy loses sharp pain sensation but retains dull pain. Which fibers are affected?
a) C fibers
b) Aδ fibers
c) Aβ fibers
d) Aα fibers
Explanation: The correct answer is Aδ fibers. Damage to thinly myelinated Aδ fibers causes loss of sharp pain and temperature discrimination, while unmyelinated C fibers still transmit burning or aching sensations, preserving slow pain response.
8) Which of the following is true regarding pain transmission by Aδ fibers?
a) They are unmyelinated
b) They transmit dull pain
c) They conduct impulses rapidly
d) They mediate visceral pain
Explanation: The correct answer is They conduct impulses rapidly. Aδ fibers are thinly myelinated, allowing faster conduction (5–30 m/s) compared to unmyelinated C fibers. They are responsible for acute, localized pain sensations from somatic structures like skin and muscles.
9) A burn patient reports persistent throbbing pain hours after injury. Which fibers are responsible?
a) Aδ fibers
b) C fibers
c) Aβ fibers
d) Aα fibers
Explanation: The correct answer is C fibers. They mediate slow, prolonged pain that persists after initial injury. This continuous pain aids in wound protection. C fibers are unmyelinated, slow-conducting, and important in chronic pain and inflammatory responses.
10) A patient with spinal cord injury loses pain and temperature sensation but retains touch and vibration. Which tract is damaged?
a) Dorsal column
b) Spinothalamic tract
c) Corticospinal tract
d) Vestibulospinal tract
Explanation: The correct answer is Spinothalamic tract. It carries pain and temperature sensations from the opposite side of the body. Its damage results in loss of these sensations below the lesion, while touch and vibration (carried by dorsal columns) remain intact.
Topic: Muscle Physiology; Subtopic: Muscle Filament Structure and Function
Keyword Definitions:
Actin: Thin filament protein forming the backbone of the I-band and interacting with myosin for muscle contraction.
Myosin: Thick filament protein responsible for generating contractile force in muscles.
Titin: Giant elastic protein anchoring myosin to the Z-line, maintaining sarcomere alignment and elasticity.
Actinin: Protein that anchors actin filaments to the Z-line in the sarcomere.
Tropomyosin: Regulatory protein covering myosin-binding sites on actin at rest.
Troponin: Calcium-binding protein complex regulating interaction between actin and myosin.
Sarcomere: Basic contractile unit of a muscle fiber, defined between two Z-lines.
Lead Question – 2014
Myosin and actin filaments are kept in place by
a) Tropomyosin
b) Troponin
c) Actinin
d) Titin
Explanation: The correct answer is Titin. Titin is a large elastic protein that connects the Z-line to the M-line, anchoring thick myosin filaments and maintaining sarcomere stability. It provides passive elasticity to muscle and helps restore resting length after contraction. Without titin, myosin alignment and muscle elasticity are severely disrupted.
1) Which protein anchors thin actin filaments to the Z-line?
a) Titin
b) Actinin
c) Troponin
d) Myomesin
Explanation: The correct answer is Actinin. α-Actinin is a structural protein found at the Z-line of sarcomeres that cross-links actin filaments, keeping them in alignment and stabilizing the Z-disc. It ensures organized contraction and uniform tension distribution during muscle shortening.
2) Which of the following proteins prevents myosin from binding to actin in a resting muscle?
a) Troponin
b) Tropomyosin
c) Titin
d) Nebulin
Explanation: The correct answer is Tropomyosin. Tropomyosin is a regulatory protein that lies along the actin filament, covering the binding sites for myosin heads. When calcium levels rise, troponin moves tropomyosin aside, allowing cross-bridge formation and contraction to occur.
3) A mutation in the titin gene primarily affects which muscle property?
a) Excitability
b) Elasticity
c) Contractility
d) Conductivity
Explanation: The correct answer is Elasticity. Titin acts as a molecular spring that contributes to passive elasticity of muscles. Mutations cause muscle weakness, cardiomyopathies, and impaired sarcomere alignment, reducing the muscle’s ability to return to its original length after stretch.
4) Which of the following is responsible for the calcium-mediated regulation of actin-myosin interaction?
a) Titin
b) Troponin
c) Actinin
d) Myomesin
Explanation: The correct answer is Troponin. The troponin complex, composed of TnI, TnT, and TnC, regulates actin-myosin binding. When calcium binds to TnC, a conformational change removes tropomyosin from actin’s binding site, enabling cross-bridge formation and muscle contraction.
5) Which part of the sarcomere shortens during muscle contraction?
a) A-band
b) I-band
c) M-line
d) Z-line
Explanation: The correct answer is I-band. During contraction, thin actin filaments slide over thick myosin filaments, reducing the length of the I-band and H-zone. The A-band remains constant, as it corresponds to the length of myosin filaments, which do not shorten.
6) A patient with a titin deficiency presents with muscle weakness and cardiac dysfunction. Which disease is likely?
a) Duchenne muscular dystrophy
b) Limb-girdle muscular dystrophy
c) Dilated cardiomyopathy
d) Myasthenia gravis
Explanation: The correct answer is Dilated cardiomyopathy. Titin mutations disrupt sarcomere integrity in cardiac muscle, leading to weakened contraction and chamber dilation. This causes reduced ejection fraction and systolic heart failure, seen in familial titinopathies.
7) Which of the following proteins determines the precise length of actin filaments in skeletal muscle?
a) Nebulin
b) Titin
c) Troponin
d) Myomesin
Explanation: The correct answer is Nebulin. Nebulin acts as a molecular ruler for actin filaments, maintaining uniform thin filament length. It stabilizes actin and contributes to efficient sarcomere contraction and alignment across muscle fibers.
8) A biopsy of skeletal muscle reveals disorganized sarcomeres with detached myosin filaments. Which protein is defective?
a) Troponin
b) Actinin
c) Titin
d) Tropomyosin
Explanation: The correct answer is Titin. Titin maintains myosin filament alignment within the sarcomere. Its deficiency causes instability of thick filaments, loss of elasticity, and disorganization, leading to myopathies characterized by weakness and structural degeneration.
9) Which ion binds to troponin to initiate muscle contraction?
a) Sodium
b) Potassium
c) Calcium
d) Magnesium
Explanation: The correct answer is Calcium. Calcium ions released from the sarcoplasmic reticulum bind to troponin C, causing tropomyosin to shift from actin-binding sites. This allows myosin heads to attach to actin, initiating cross-bridge cycling and muscle contraction.
10) During relaxation of muscle fibers, which mechanism helps restore calcium levels in the sarcoplasmic reticulum?
a) SERCA pump
b) Na⁺/K⁺ ATPase
c) Voltage-gated channels
d) Ryanodine receptor
Explanation: The correct answer is SERCA pump. The sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase (SERCA) actively pumps calcium back into the SR after contraction, reducing cytoplasmic calcium levels, detaching cross-bridges, and promoting muscle relaxation.
Chapter: Neurophysiology; Topic: Cerebellum; Subtopic: Cerebellar Neuronal Connections
Keyword Definitions:
Cerebellum: Part of the hindbrain that coordinates voluntary movements, posture, and balance.
Climbing fibres: Afferents from the inferior olivary nucleus that synapse directly with Purkinje cells.
Mossy fibres: Afferents from the spinal cord, vestibular nuclei, and pontine nuclei that excite granule cells.
Purkinje cells: Large inhibitory neurons of the cerebellar cortex projecting to deep cerebellar nuclei.
Lead Question - 2014
True about cerebellar neuronal connections?
a) Climbing fibres from inferior olivary nucleus
b) Mossy fibres from inferior olivary nucleus
c) Climbing fibres are inhibitory to Purkinje cells
d) Mossy fibres are inhibitory to Purkinje cells
Explanation: Climbing fibres originate exclusively from the inferior olivary nucleus and form powerful excitatory synapses on Purkinje cells, each Purkinje cell receiving input from a single climbing fibre. Mossy fibres arise from multiple sources such as the spinal cord and pontine nuclei and excite granule cells indirectly. Hence, the correct answer is (a) Climbing fibres from inferior olivary nucleus.
1) The neurotransmitter released by Purkinje cells is:
a) GABA
b) Glutamate
c) Dopamine
d) Serotonin
Explanation: Purkinje cells are inhibitory neurons that release GABA (gamma-aminobutyric acid) onto deep cerebellar nuclei. They play a crucial role in modulating cerebellar output, ensuring smooth and coordinated motor activity. Their inhibitory nature helps prevent overactivation of motor pathways. The correct answer is (a) GABA.
2) Which structure acts as the major output of the cerebellum?
a) Purkinje cells
b) Deep cerebellar nuclei
c) Inferior olivary nucleus
d) Granule cells
Explanation: The cerebellum’s output is mediated through the deep cerebellar nuclei, which receive inhibitory input from Purkinje cells and send excitatory signals to motor centers in the brainstem and thalamus. These nuclei are dentate, emboliform, globose, and fastigial. Hence, the correct answer is (b) Deep cerebellar nuclei.
3) Lesion of the cerebellar hemisphere leads to:
a) Intention tremor
b) Resting tremor
c) Rigidity
d) Flaccidity
Explanation: Lesions of the cerebellar hemisphere affect coordination on the ipsilateral side of the body, causing intention tremor, dysmetria, and dysdiadochokinesia. These are hallmark signs of cerebellar dysfunction distinct from extrapyramidal disorders that cause resting tremor or rigidity. The correct answer is (a) Intention tremor.
4) Mossy fibres synapse with which cells?
a) Purkinje cells
b) Golgi cells
c) Granule cells
d) Stellate cells
Explanation: Mossy fibres synapse on granule cells in the cerebellar cortex, which then project via parallel fibres to Purkinje cells. This indirect pathway modulates cerebellar output and integrates sensory and motor information. Therefore, the correct answer is (c) Granule cells.
5) Climbing fibre activity produces:
a) Simple spikes
b) Complex spikes
c) EPSPs
d) IPSPs
Explanation: Climbing fibres from the inferior olivary nucleus generate “complex spikes” in Purkinje cells due to multiple excitatory synapses. These spikes differ from the “simple spikes” produced by mossy fibre–granule cell pathways. Complex spikes are essential for motor learning. Hence, the correct answer is (b) Complex spikes.
6) A 32-year-old patient presents with loss of coordination and inability to perform rapid alternating movements. Which cerebellar area is most likely affected?
a) Vestibulocerebellum
b) Spinocerebellum
c) Cerebrocerebellum
d) Flocculonodular lobe
Explanation: The cerebrocerebellum, mainly the lateral hemispheres, coordinates skilled and sequential movements. Its lesion leads to dysdiadochokinesia and loss of fine motor control. Vestibulocerebellum deals with balance, and spinocerebellum with posture. The correct answer is (c) Cerebrocerebellum.
7) Which tract conveys proprioceptive information to the cerebellum?
a) Corticospinal tract
b) Spinothalamic tract
c) Spinocerebellar tract
d) Rubrospinal tract
Explanation: The spinocerebellar tracts (dorsal and ventral) transmit unconscious proprioceptive information to the cerebellum for coordination and posture control. These tracts enable real-time correction of movement errors. Therefore, the correct answer is (c) Spinocerebellar tract.
8) In cerebellar lesions, which side of the body is affected?
a) Contralateral
b) Bilateral
c) Ipsilateral
d) Alternate
Explanation: Each cerebellar hemisphere controls coordination of movements on the same (ipsilateral) side of the body due to double crossing of pathways. Therefore, cerebellar lesions produce ipsilateral deficits. The correct answer is (c) Ipsilateral.
9) In a patient with cerebellar damage, eye movements are erratic. Which area is most likely involved?
a) Vermis
b) Flocculonodular lobe
c) Dentate nucleus
d) Fastigial nucleus
Explanation: The flocculonodular lobe, part of the vestibulocerebellum, maintains equilibrium and coordinates eye movements via vestibular nuclei. Lesions cause nystagmus and postural instability. Hence, the correct answer is (b) Flocculonodular lobe.
10) A patient exhibits ataxia after chronic alcoholism. Which cerebellar region is typically damaged?
a) Vermis
b) Lateral hemisphere
c) Flocculonodular lobe
d) Dentate nucleus
Explanation: Chronic alcoholism often causes degeneration of the cerebellar vermis, leading to truncal ataxia and gait instability. The vermis regulates posture and balance. Therefore, the correct answer is (a) Vermis.
Chapter: Neurophysiology; Topic: Synaptic Transmission; Subtopic: Post-Tetanic Potentiation
Keyword Definitions:
Post-tetanic potentiation: A short-term increase in synaptic strength following high-frequency stimulation, due to residual calcium accumulation in the presynaptic terminal.
Synaptic transmission: Process by which neurons communicate across synapses through neurotransmitter release.
Calcium ions (Ca++): Essential ions that trigger neurotransmitter vesicle fusion with the presynaptic membrane.
Neurotransmitter release: The exocytosis of chemical messengers like acetylcholine or glutamate from nerve terminals.
Lead Question - 2014
Post-tetanic potentiation is due to -
a) Hyperpolarization of muscle fibres
b) Rapid K+ efflux
c) Increased availability of Ca++
d) Rapid Na+ influx
Explanation: Post-tetanic potentiation occurs when repetitive stimulation leads to an increased influx of calcium ions into the presynaptic terminal. The residual calcium enhances neurotransmitter release during subsequent stimuli, resulting in stronger postsynaptic responses. This mechanism is important in short-term memory and synaptic plasticity. Hence, the correct answer is (c) Increased availability of Ca++.
1) The primary site of calcium accumulation during post-tetanic potentiation is:
a) Postsynaptic membrane
b) Presynaptic terminal
c) Synaptic cleft
d) Dendritic spines
Explanation: Post-tetanic potentiation is caused by accumulation of calcium within the presynaptic terminal after high-frequency stimulation. This calcium facilitates additional neurotransmitter release with subsequent impulses, enhancing synaptic transmission transiently. The postsynaptic response increases due to more transmitter molecules binding to receptors. Thus, the correct answer is (b) Presynaptic terminal.
2) Which of the following best describes the time course of post-tetanic potentiation?
a) Lasts milliseconds
b) Lasts seconds to minutes
c) Lasts hours
d) Permanent
Explanation: Post-tetanic potentiation typically lasts for several seconds to a few minutes after the tetanic stimulation ends. It reflects short-term synaptic plasticity rather than long-term potentiation, which lasts hours or days. The transient increase in neurotransmitter release fades as presynaptic calcium levels return to normal. The correct answer is (b) Lasts seconds to minutes.
3) A patient with Lambert-Eaton myasthenic syndrome shows decreased post-tetanic potentiation. This is due to:
a) Defect in acetylcholine receptors
b) Defect in presynaptic calcium channels
c) Excessive acetylcholine degradation
d) Overactive sodium channels
Explanation: Lambert-Eaton myasthenic syndrome (LEMS) involves autoantibodies against presynaptic voltage-gated calcium channels, impairing calcium influx and thus neurotransmitter release. This reduces post-tetanic potentiation. Unlike myasthenia gravis, LEMS primarily affects presynaptic mechanisms. Hence, the correct answer is (b) Defect in presynaptic calcium channels.
4) During post-tetanic potentiation, enhanced neurotransmitter release is primarily due to:
a) Increased vesicle number
b) Increased presynaptic calcium
c) Increased postsynaptic receptors
d) Reduced potassium conductance
Explanation: The accumulation of calcium in the presynaptic terminal increases the probability of synaptic vesicle fusion with the presynaptic membrane, thereby increasing neurotransmitter release. This transient enhancement of synaptic efficacy defines post-tetanic potentiation. Hence, the correct answer is (b) Increased presynaptic calcium.
5) Which ion’s accumulation is responsible for post-tetanic potentiation?
a) Na+
b) K+
c) Cl−
d) Ca++
Explanation: Calcium ions (Ca++) accumulate in the presynaptic terminal during repeated stimulation, enhancing neurotransmitter release. This transient elevation causes stronger postsynaptic potentials upon subsequent impulses, which is the hallmark of post-tetanic potentiation. The correct answer is (d) Ca++.
6) A 42-year-old man with chronic fatigue exhibits improved muscle contraction after repetitive nerve stimulation. This is characteristic of:
a) Myasthenia gravis
b) Lambert-Eaton syndrome
c) Botulism
d) Duchenne muscular dystrophy
Explanation: In Lambert-Eaton syndrome, repetitive nerve stimulation transiently improves muscle strength due to facilitation of calcium entry and enhanced acetylcholine release—reflecting post-tetanic potentiation. In contrast, myasthenia gravis shows fatigability without facilitation. Hence, the correct answer is (b) Lambert-Eaton syndrome.
7) Post-tetanic potentiation is an example of:
a) Long-term potentiation
b) Short-term synaptic plasticity
c) Synaptic depression
d) Neural adaptation
Explanation: Post-tetanic potentiation represents short-term synaptic plasticity where transient increases in neurotransmitter release enhance synaptic strength for seconds to minutes. It differs from long-term potentiation (LTP), which involves gene expression and structural changes. The correct answer is (b) Short-term synaptic plasticity.
8) Which process terminates post-tetanic potentiation?
a) Calcium sequestration by mitochondria
b) Increased neurotransmitter release
c) Sodium influx
d) Potassium efflux
Explanation: The decline of post-tetanic potentiation occurs as intracellular calcium is pumped back into the endoplasmic reticulum or sequestered by mitochondria, restoring baseline neurotransmitter release rates. The temporary nature of calcium elevation explains why potentiation is short-lived. The correct answer is (a) Calcium sequestration by mitochondria.
9) Which synapse commonly exhibits post-tetanic potentiation?
a) Neuromuscular junction
b) Retinal synapses
c) Cerebellar synapses
d) Autonomic ganglia
Explanation: Post-tetanic potentiation is well-documented in cerebellar and hippocampal synapses, where repetitive activation strengthens transmission for seconds to minutes. This phenomenon underlies short-term learning and coordination adjustments. Hence, the correct answer is (c) Cerebellar synapses.
10) A patient’s EMG shows enhanced amplitude after rapid nerve stimulation. This finding suggests:
a) Myasthenia gravis
b) Lambert-Eaton myasthenic syndrome
c) Multiple sclerosis
d) Motor neuron disease
Explanation: Enhanced EMG amplitude after rapid stimulation is a hallmark of post-tetanic potentiation, typical in Lambert-Eaton syndrome. It reflects increased calcium entry into presynaptic terminals during repetitive activity, improving acetylcholine release and muscle contraction. The correct answer is (b) Lambert-Eaton myasthenic syndrome.
Chapter: Neurophysiology; Topic: Somatosensory System; Subtopic: Cortical Representation (Sensory Homunculus)
Keyword Definitions:
Somatosensory cortex: The region of the cerebral cortex responsible for processing sensory input from various parts of the body.
Sensory homunculus: A cortical map showing how much of the somatosensory cortex is devoted to sensations from each body region.
Proprioception: The sense of position and movement of body parts.
Cortical representation: The area of the cerebral cortex that corresponds to sensory input from specific body parts, proportional to sensitivity rather than size.
Lead Question - 2014
Which of the following has small representation in somatosensory area of cerebral cortex?
a) Lips
b) Thumb/fingers
c) Tongue
d) Trunk
Explanation: The somatosensory cortex (Brodmann’s areas 3, 1, and 2) has disproportionate representation of different body parts, depending on their sensory precision. Highly sensitive areas like lips, tongue, and fingers occupy large cortical areas, while less sensitive parts like the trunk and thigh have small representation. Hence, the correct answer is (d) Trunk.
1) Which lobe of the brain contains the primary somatosensory cortex?
a) Frontal lobe
b) Parietal lobe
c) Temporal lobe
d) Occipital lobe
Explanation: The primary somatosensory cortex lies in the postcentral gyrus of the parietal lobe, corresponding to Brodmann’s areas 3, 1, and 2. It processes tactile, proprioceptive, and nociceptive sensations from the body surface and deeper tissues. The correct answer is (b) Parietal lobe.
2) A 45-year-old patient with a lesion in the right postcentral gyrus may show loss of sensation in:
a) Right hand
b) Left hand
c) Both hands
d) Lower limbs only
Explanation: The somatosensory cortex receives contralateral sensory input; hence, a lesion in the right postcentral gyrus results in sensory deficits on the left side of the body, typically affecting the hand and face depending on lesion location. Therefore, the correct answer is (b) Left hand.
3) Which area of the body has the largest cortical representation in the sensory homunculus?
a) Trunk
b) Lips
c) Forearm
d) Thigh
Explanation: The sensory homunculus reflects density of sensory receptors rather than body size. The lips and tongue, rich in tactile receptors, occupy large cortical representation, allowing fine discrimination. In contrast, areas like the trunk and thigh have limited sensory input. Hence, the correct answer is (b) Lips.
4) Which Brodmann areas correspond to the primary somatosensory cortex?
a) 17
b) 4
c) 3, 1, 2
d) 22
Explanation: Brodmann’s areas 3, 1, and 2, located on the postcentral gyrus, constitute the primary somatosensory cortex. These areas receive projections from the thalamus and process tactile, pain, temperature, and proprioceptive sensations. Hence, the correct answer is (c) 3, 1, 2.
5) Which of the following body parts has bilateral cortical representation for sensation?
a) Face
b) Lips
c) Genitalia
d) Hand
Explanation: While most somatosensory input is contralateral, certain midline structures like the genitalia, pharynx, and parts of the oral cavity have bilateral cortical representation to preserve sensory awareness on both sides. The correct answer is (c) Genitalia.
6) A 50-year-old man with a parietal lobe stroke is unable to recognize objects by touch (astereognosis). The lesion likely involves:
a) Primary motor cortex
b) Secondary somatosensory area
c) Visual cortex
d) Cerebellum
Explanation: Astereognosis—loss of tactile object recognition—occurs when the secondary somatosensory cortex (area 5 and 7) in the parietal lobe is affected. Primary sensory input remains intact, but higher processing for object interpretation is lost. Hence, the correct answer is (b) Secondary somatosensory area.
7) The thalamic nucleus that projects to the primary somatosensory cortex is:
a) Ventral posterior nucleus
b) Medial geniculate body
c) Lateral geniculate body
d) Ventral anterior nucleus
Explanation: The ventral posterior nucleus of the thalamus transmits somatosensory information to Brodmann’s areas 3, 1, and 2. The ventral posterior lateral (VPL) handles body input, and ventral posterior medial (VPM) handles face input. Thus, the correct answer is (a) Ventral posterior nucleus.
8) Lesion of the right parietal association cortex causes which clinical sign?
a) Aphasia
b) Left-sided neglect
c) Right-sided neglect
d) Agraphia
Explanation: Damage to the right parietal association area causes left-sided spatial neglect due to impaired perception of the contralateral environment. Patients may ignore the left side of their body or surroundings. The correct answer is (b) Left-sided neglect.
9) A patient cannot localize the source of pain after cortical injury. This indicates involvement of:
a) Thalamus
b) Primary somatosensory cortex
c) Cerebellum
d) Hippocampus
Explanation: Localization of pain depends on cortical processing in the primary somatosensory area. A lesion here impairs the ability to identify and localize painful stimuli, though the pain perception itself remains intact. Thus, the correct answer is (b) Primary somatosensory cortex.
10) In the sensory homunculus, which body part lies most medially on the cortex?
a) Face
b) Hand
c) Leg
d) Tongue
Explanation: In the cortical sensory map, the leg and foot are represented medially on the paracentral lobule, while the face and hand are located more laterally. This somatotopic organization corresponds to the body layout on the sensory cortex. The correct answer is (c) Leg.
Chapter: Cardiovascular Physiology; Topic: Cardiac Electrophysiology; Subtopic: Resting Membrane Potential in Cardiac Muscle
Keyword Definitions:
Resting Membrane Potential: The electrical potential difference across the cell membrane during rest, caused by unequal ion distribution.
Cardiac Muscle: Specialized involuntary striated muscle responsible for rhythmic contraction of the heart.
Depolarization: Process where the cell becomes less negative due to sodium ion influx.
Potassium Leak Channels: Channels allowing passive K⁺ efflux, maintaining the resting potential.
Lead Question - 2014
Resting membrane potential in cardiac muscle?
a) -70 mV
b) +70 mV
c) -90 mV
d) +90 mV
Explanation: The resting membrane potential of cardiac muscle fibers is around -90 mV, mainly due to high K⁺ permeability and low Na⁺ permeability. This negative potential maintains the excitability of cardiac myocytes. During depolarization, Na⁺ influx reverses polarity, initiating the action potential. Thus, the correct answer is c) -90 mV.
1) The main ion responsible for maintaining resting membrane potential is?
a) Sodium
b) Calcium
c) Potassium
d) Chloride
Explanation: Potassium ions (K⁺) play the most significant role in maintaining the resting membrane potential. The cell membrane is highly permeable to K⁺ due to leak channels, allowing efflux that makes the interior negative. This electrochemical balance is vital for cardiac muscle excitability. The correct answer is c) Potassium.
2) Which phase of cardiac action potential corresponds to repolarization?
a) Phase 0
b) Phase 1
c) Phase 2
d) Phase 3
Explanation: Repolarization occurs during Phase 3, characterized by the efflux of K⁺ ions, restoring the membrane potential toward -90 mV. This prepares the cardiac cell for the next depolarization cycle. The process ensures rhythmic contractions of the heart. Therefore, the correct answer is d) Phase 3.
3) Which ion’s influx is responsible for the plateau phase in cardiac muscle action potential?
a) Na⁺
b) K⁺
c) Ca²⁺
d) Cl⁻
Explanation: The plateau phase (Phase 2) results from the slow influx of Ca²⁺ through L-type calcium channels, balancing K⁺ efflux. This prolongs depolarization, ensuring efficient contraction and coordinated ejection of blood from the heart chambers. Hence, the correct answer is c) Ca²⁺.
4) Which of the following best describes the sodium-potassium pump’s role in cardiac cells?
a) Moves Na⁺ inside and K⁺ outside
b) Moves Na⁺ outside and K⁺ inside
c) Moves both ions inside
d) Moves both ions outside
Explanation: The sodium-potassium ATPase pump maintains ionic gradients by pumping 3 Na⁺ ions out and 2 K⁺ ions into the cardiac cell. This active transport maintains the negative resting potential and prevents depolarization under resting conditions. The correct answer is b) Moves Na⁺ outside and K⁺ inside.
5) In ischemic heart tissue, resting membrane potential becomes less negative due to:
a) Decreased Na⁺ influx
b) Increased K⁺ efflux
c) Decreased ATP production
d) Increased calcium uptake
Explanation: During ischemia, reduced ATP impairs the Na⁺/K⁺ ATPase pump, leading to K⁺ accumulation inside cells and Na⁺ retention, making the resting potential less negative. This reduces excitability and conduction velocity, predisposing to arrhythmias. The correct answer is c) Decreased ATP production.
6) A patient with hyperkalemia is most likely to exhibit:
a) Hyperpolarization
b) Depolarization
c) Increased membrane potential
d) Enhanced conduction
Explanation: Hyperkalemia decreases the K⁺ gradient across the cardiac cell membrane, causing partial depolarization. This inactivates Na⁺ channels, slowing conduction and potentially leading to arrhythmias or cardiac arrest. Hence, the correct answer is b) Depolarization.
7) Which of the following cardiac cells shows the most stable resting membrane potential?
a) SA node
b) AV node
c) Ventricular myocytes
d) Purkinje fibers
Explanation: Ventricular myocytes possess the most stable resting membrane potential around -90 mV, showing no spontaneous depolarization. In contrast, SA and AV nodes exhibit pacemaker activity with unstable potentials. Thus, the correct answer is c) Ventricular myocytes.
8) Which ion primarily determines the cardiac action potential threshold?
a) K⁺
b) Na⁺
c) Ca²⁺
d) Cl⁻
Explanation: Sodium ions (Na⁺) determine the threshold potential in cardiac cells. When Na⁺ channels open, rapid influx depolarizes the membrane, triggering the action potential. This excitability threshold ensures coordinated cardiac contraction. Hence, the correct answer is b) Na⁺.
9) Which cardiac ion channel blocker prolongs the plateau phase?
a) Calcium channel blocker
b) Potassium channel blocker
c) Sodium channel blocker
d) Beta blocker
Explanation: Potassium channel blockers (Class III antiarrhythmics) prolong the plateau and repolarization phases by reducing K⁺ efflux. This increases the duration of the action potential and refractory period, stabilizing rhythm. The correct answer is b) Potassium channel blocker.
10) During which phase of cardiac action potential is Na⁺ channel inactivation complete?
a) Phase 0
b) Phase 1
c) Phase 2
d) Phase 3
Explanation: Na⁺ channel inactivation is complete by the end of Phase 1, shortly after the rapid depolarization of Phase 0. This ensures unidirectional conduction and prevents premature excitation. Thus, the correct answer is b) Phase 1.
Chapter: Nervous System Physiology; Topic: Autonomic Nervous System; Subtopic: Neurotransmitters of Sympathetic and Parasympathetic Systems
Keyword Definitions:
Noradrenaline (Norepinephrine): A catecholamine neurotransmitter released mainly by postganglionic sympathetic fibers, except in sweat glands.
Postganglionic Fibers: Neurons extending from autonomic ganglia to target organs.
Sympathetic Nervous System: Division of the autonomic nervous system responsible for “fight or flight” responses.
Parasympathetic Nervous System: Division promoting “rest and digest” functions using acetylcholine as neurotransmitter.
Lead Question - 2014
Noradrenaline is major neurotransmitter in?
a) Postganglionic parasympathetic fibres
b) Postganglionic sympathetic fibres except in sweat glands
c) Autonomic ganglia
d) Preganglionic autonomic fibres
Explanation: Noradrenaline is the principal neurotransmitter released by postganglionic sympathetic fibers, except those innervating sweat glands, which release acetylcholine. It acts via adrenergic receptors to increase heart rate, blood pressure, and glucose availability during stress. Hence, the correct answer is b) Postganglionic sympathetic fibres except in sweat glands.
1) Which neurotransmitter is released by preganglionic sympathetic neurons?
a) Dopamine
b) Acetylcholine
c) Noradrenaline
d) Serotonin
Explanation: Preganglionic neurons of both sympathetic and parasympathetic systems release acetylcholine, which acts on nicotinic receptors in autonomic ganglia. This cholinergic signaling ensures transmission before the effector organ response. Hence, the correct answer is b) Acetylcholine.
2) Sweat glands are unique because their postganglionic sympathetic fibers release:
a) Dopamine
b) Acetylcholine
c) Noradrenaline
d) Serotonin
Explanation: Sweat glands are an exception in the sympathetic system as their postganglionic fibers release acetylcholine rather than noradrenaline. This neurotransmitter acts on muscarinic receptors to promote sweating, crucial for thermoregulation. Therefore, the correct answer is b) Acetylcholine.
3) Which enzyme converts dopamine to noradrenaline in sympathetic nerve endings?
a) Dopamine decarboxylase
b) Monoamine oxidase
c) Dopamine β-hydroxylase
d) Tyrosine hydroxylase
Explanation: Dopamine β-hydroxylase catalyzes the conversion of dopamine into noradrenaline within vesicles of sympathetic neurons. This enzyme is essential for catecholamine synthesis and proper sympathetic neurotransmission. Thus, the correct answer is c) Dopamine β-hydroxylase.
4) Which receptor subtype does noradrenaline primarily act on in the heart?
a) α1 receptors
b) β1 receptors
c) β2 receptors
d) α2 receptors
Explanation: Noradrenaline predominantly acts on β1 adrenergic receptors in the heart, increasing heart rate, contractility, and cardiac output. This sympathetic activation supports the body’s fight-or-flight response. The correct answer is b) β1 receptors.
5) Which neurotransmitter is deficient in a patient with postganglionic sympathetic denervation?
a) Acetylcholine
b) Noradrenaline
c) Dopamine
d) Glutamate
Explanation: Postganglionic sympathetic denervation leads to a deficiency of noradrenaline, resulting in loss of sympathetic tone, hypotension, and impaired stress response. This condition affects adrenergic receptor-mediated activities. Therefore, the correct answer is b) Noradrenaline.
6) A patient with pheochromocytoma will show elevated levels of:
a) Noradrenaline
b) Acetylcholine
c) GABA
d) Serotonin
Explanation: Pheochromocytoma, a tumor of the adrenal medulla, causes excessive secretion of catecholamines, mainly noradrenaline and adrenaline. It results in hypertension, palpitations, and sweating. Elevated plasma or urinary metanephrines confirm the diagnosis. Thus, the correct answer is a) Noradrenaline.
7) Which neurotransmitter acts on nicotinic receptors in autonomic ganglia?
a) Acetylcholine
b) Noradrenaline
c) Adrenaline
d) Dopamine
Explanation: Acetylcholine is the neurotransmitter acting on nicotinic receptors within autonomic ganglia, facilitating synaptic transmission between preganglionic and postganglionic neurons. This cholinergic signal is crucial for both sympathetic and parasympathetic systems. The correct answer is a) Acetylcholine.
8) A patient treated with reserpine shows decreased sympathetic activity because it:
a) Inhibits acetylcholine release
b) Depletes noradrenaline from vesicles
c) Blocks adrenergic receptors
d) Enhances dopamine synthesis
Explanation: Reserpine inhibits vesicular monoamine transporter (VMAT), preventing storage of noradrenaline in synaptic vesicles. This depletion reduces sympathetic transmission and lowers blood pressure. The correct answer is b) Depletes noradrenaline from vesicles.
9) Which of the following drugs increases noradrenaline levels by inhibiting its reuptake?
a) Cocaine
b) Atropine
c) Clonidine
d) Propranolol
Explanation: Cocaine inhibits the reuptake of noradrenaline and dopamine at synaptic clefts, leading to increased sympathetic stimulation, euphoria, and hypertension. This pharmacologic effect explains cocaine’s sympathomimetic actions. Therefore, the correct answer is a) Cocaine.
10) Which of the following symptoms is NOT mediated by noradrenaline release?
a) Increased heart rate
b) Pupil dilation
c) Bronchodilation
d) Salivation
Explanation: Noradrenaline mediates sympathetic effects like increased heart rate and pupil dilation but does not cause salivation, which is a parasympathetic (acetylcholine-mediated) response. Hence, the correct answer is d) Salivation.
Chapter: Nervous System; Topic: Neurotrophic Factors; Subtopic: Brain-Derived Neurotrophic Factor (BDNF) and its Receptors
Keyword Definitions:
• BDNF: Brain-Derived Neurotrophic Factor, a protein promoting neuron survival and synaptic plasticity.
• TrK Receptors: Tyrosine kinase receptors mediating neurotrophin signaling.
• Neurotrophins: Family of growth factors essential for nervous system development.
• Synaptic Plasticity: Ability of synapses to strengthen or weaken over time.
• Neuronal Survival: Maintenance of neurons by growth factors like BDNF.
• Neurodegeneration: Progressive loss of neuron function and structure.
• TrK-B: Specific receptor for BDNF mediating neuronal growth and differentiation.
Lead Question – 2014
Receptor for BDNF?
a) TrK-A
b) TrK-B
c) TrK-C
d) None
Explanation: Brain-Derived Neurotrophic Factor (BDNF) primarily binds to TrK-B receptors, initiating intracellular signaling that promotes neuronal survival, differentiation, and synaptic plasticity. Unlike NGF that binds to TrK-A or NT-3 that binds to TrK-C, BDNF is specific for TrK-B. This receptor plays a vital role in learning, memory, and neuroprotection in the central nervous system. Answer: (b) TrK-B.
1. Which of the following neurotrophins primarily binds to TrK-A receptor?
a) Nerve Growth Factor (NGF)
b) BDNF
c) Neurotrophin-3
d) Neurotrophin-4
Explanation: NGF (Nerve Growth Factor) binds specifically to TrK-A receptor. This interaction promotes neuronal differentiation and maintenance of sympathetic and sensory neurons. TrK-A activation triggers MAP kinase and PI3K pathways, enhancing cell survival and neurite growth. BDNF and NT-3 act on TrK-B and TrK-C respectively. Answer: (a) NGF.
2. BDNF plays a crucial role in which of the following processes?
a) Liver regeneration
b) Bone mineralization
c) Synaptic plasticity
d) Hormone synthesis
Explanation: BDNF is essential for synaptic plasticity—the ability of synapses to adapt during learning and memory formation. It strengthens neuronal connections by enhancing neurotransmitter release and dendritic growth. This function underlies cognitive functions such as memory consolidation and learning adaptability. Answer: (c) Synaptic plasticity.
3. TrK-C receptor mainly binds with which neurotrophin?
a) NGF
b) NT-3
c) NT-4
d) BDNF
Explanation: TrK-C receptor has high affinity for Neurotrophin-3 (NT-3), which regulates neuronal survival and axonal growth in both central and peripheral nervous systems. It also cross-reacts weakly with TrK-A and TrK-B. Activation of TrK-C triggers signaling cascades crucial for neuron differentiation. Answer: (b) NT-3.
4. A 45-year-old patient with depression shows decreased hippocampal volume. Which factor deficiency is most likely responsible?
a) NGF
b) BDNF
c) Dopamine
d) ACTH
Explanation: Decreased BDNF levels are linked with depression and reduced hippocampal neurogenesis. BDNF supports survival and growth of neurons in the hippocampus, enhancing memory and emotional regulation. Antidepressant therapy increases BDNF expression, promoting neuroplasticity and recovery. Answer: (b) BDNF.
5. Which receptor mediates the effect of Nerve Growth Factor (NGF)?
a) TrK-A
b) TrK-B
c) TrK-C
d) TrK-D
Explanation: NGF exerts its biological effects mainly through TrK-A receptor. Activation of TrK-A promotes neuronal differentiation, maintenance, and survival in sympathetic and sensory neurons. This receptor is vital for pain perception and autonomic nervous system function. Answer: (a) TrK-A.
6. A patient recovering from stroke demonstrates improved motor recovery due to increased neurotrophin release. Which receptor is primarily involved?
a) TrK-A
b) TrK-B
c) TrK-C
d) p75 receptor
Explanation: TrK-B receptor mediates BDNF’s neuroprotective effects after stroke, promoting neuronal repair and synaptic remodeling. Enhanced BDNF–TrK-B signaling contributes to neurogenesis and recovery of motor functions through activation of intracellular cascades like MAPK and PI3K pathways. Answer: (b) TrK-B.
7. Which neurotrophin deficiency is most commonly linked to Alzheimer’s disease?
a) NGF
b) BDNF
c) NT-3
d) NT-4
Explanation: BDNF deficiency contributes to synaptic loss and neuronal degeneration in Alzheimer’s disease. Reduced BDNF-TrK-B signaling impairs synaptic plasticity, leading to cognitive decline. Restoring BDNF levels improves neuronal survival and cognitive function, highlighting its therapeutic potential in neurodegenerative disorders. Answer: (b) BDNF.
8. TrK-B receptor activation primarily stimulates which intracellular signaling pathway?
a) JAK-STAT
b) MAPK and PI3K-Akt
c) TGF-beta
d) Wnt-beta catenin
Explanation: TrK-B receptor activation triggers MAPK and PI3K-Akt pathways, promoting cell survival, synaptic plasticity, and neuronal differentiation. These cascades mediate neurotrophic effects of BDNF, ensuring neuronal health and adaptive brain function. Answer: (b) MAPK and PI3K-Akt.
9. Which of the following receptors binds both BDNF and NT-4?
a) TrK-A
b) TrK-B
c) TrK-C
d) p75 receptor
Explanation: Both BDNF and NT-4 share the same high-affinity receptor, TrK-B. Binding activates neuroprotective signaling pathways that enhance synaptic function and plasticity. These pathways play key roles in development and maintenance of the nervous system. Answer: (b) TrK-B.
10. A 32-year-old woman with long-term antidepressant use shows increased hippocampal BDNF expression. Which mechanism best explains this?
a) Reduced cortisol binding
b) Enhanced BDNF-TrK-B signaling
c) Decreased dopamine reuptake
d) Blocked serotonin degradation
Explanation: Chronic antidepressant use enhances BDNF-TrK-B signaling, improving neurogenesis and synaptic remodeling in the hippocampus. This molecular adaptation restores neural circuitry, alleviating depressive symptoms and improving cognitive performance. Answer: (b) Enhanced BDNF-TrK-B signaling.