Synaptic Transmission — MCQs
Which of the following is true regarding Na+ (sodium) ions?
Absolute refractoriness of a neuron is due to?
Mechanism of action of d-tubocurarine is:
Sequence the events in neuromuscular action potential conduction: 1. Sodium channels open in the end plate 2. Calcium enters at the nerve terminal 3. Release of acetylcholine
Which of the following is true about Lambert-Eaton syndrome?
Match the following: A) Glossopharyngeal nerve B) Spinal accessory nerve C) Facial nerve D) Mandibular nerve 1) Shrugging of shoulder 2) Touch sensation from the posterior one-third of the tongue 3) Chewing 4) Taste from the anterior two-thirds of the tongue
Primary afferent fibers secrete which nociceptive substance at the dorsal horn?
Which of the following is true regarding Lambert-Eaton myasthenic syndrome?
The mechanism of action of botulinum toxin A is best described by:
Retinal cells which secrete acetylcholine are:
Synaptic Transmission Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is true regarding Na+ (sodium) ions?
- A. Does not help other ions in transport
- B. Responsible for depolarization (Correct Answer)
- C. Responsible for the resting membrane potential
- D. Sodium ion is responsible for Donnan effect
Explanation: ***Responsible for depolarization*** - The rapid influx of **Na+ ions** into the cell through voltage-gated sodium channels is the primary event that causes **depolarization** during an action potential. - This influx makes the inside of the cell more positive, shifting the membrane potential from negative toward positive values. *Sodium ion is responsible for Donnan effect* - The **Donnan effect** describes the unequal distribution of permeable ions across a semi-permeable membrane due to the presence of impermeant charged molecules (e.g., proteins). - **Na+ ions are small, permeable ions** - they do not create the Donnan effect. The effect is caused by large, non-diffusible charged molecules like proteins, not by sodium ions. *Does not help other ions in transport* - The **sodium-potassium pump (Na+/K+-ATPase)** actively transports Na+ out of the cell and K+ into the cell, maintaining their concentration gradients. - These Na+ gradients are crucial for **secondary active transport**, where the energy from Na+ moving down its electrochemical gradient is used to move other ions (e.g., in Na+-glucose cotransport) or molecules against their gradients. *Responsible for the resting membrane potential* - The **resting membrane potential** is primarily established by the differential permeability of the membrane to K+ ions and the activity of the Na+/K+-ATPase. - While Na+ leaking into the cell contributes slightly, the dominant factor is the efflux of **K+ ions** through leak channels, as the membrane is much more permeable to K+ than to Na+ at rest.
Question 2: Absolute refractoriness of a neuron is due to?
- A. Hyperpolarization of Cl channels
- B. Opening of rectifier K+ channels
- C. Closure of activated Na channels
- D. Inactivation of Na channels (Correct Answer)
Explanation: ***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.
Question 3: Mechanism of action of d-tubocurarine is:
- A. Competitive, nondepolarizing block at the Nm cholinergic receptor (Correct Answer)
- B. Noncompetitive, depolarizing block at the Nm cholinergic receptor
- C. Non-competitive, nondepolarizing block at the Nm cholinergic receptor
- D. Competitive, depolarizing block at the Nm cholinergic receptor
Explanation: ***Competitive, nondepolarizing block at the Nm cholinergic receptor*** - **d-tubocurarine** acts as a **competitive antagonist** at the **nicotinic muscle (Nm) cholinergic receptors** on the motor endplate. - It competes with **acetylcholine (ACh)** for binding sites, preventing ACh from activating the receptor and causing **muscle paralysis** without depolarization. *Noncompetitive, depolarizing block at the Nm cholinergic receptor* - This describes the mechanism of action of **depolarizing neuromuscular blockers** like **succinylcholine**, which first *depolarize* the motor endplate before causing paralysis. - d-tubocurarine does not cause initial depolarization; it directly blocks the receptor. *Non-competitive, nondepolarizing block at the Nm cholinergic receptor* - While d-tubocurarine is **nondepolarizing**, it is a **competitive antagonist**, not a non-competitive one. - A non-competitive block would involve binding to a different site on the receptor or an associated ion channel, altering receptor function indirectly. *Competitive, depolarizing block at the Nm cholinergic receptor* - This option incorrectly combines the concepts, as **depolarizing blockers** like succinylcholine act initially by **depolarizing** the endplate, whereas d-tubocurarine is purely a **nondepolarizing** agent. - The "competitive" aspect would be true for the binding of ACh to its site on a depolarizing agent, but the effect of d-tubocurarine is simply to block, not depolarize.
Question 4: Sequence the events in neuromuscular action potential conduction: 1. Sodium channels open in the end plate 2. Calcium enters at the nerve terminal 3. Release of acetylcholine
- A. $1 \rightarrow 2 \rightarrow 3$
- B. $1 \rightarrow 3 \rightarrow 2$
- C. $3 \rightarrow 2 \rightarrow 1$
- D. $2 \rightarrow 3 \rightarrow 1$ (Correct Answer)
Explanation: ***Correct: $2 \rightarrow 3 \rightarrow 1$*** - **Calcium entry at the nerve terminal** is the initial trigger - when an action potential reaches the presynaptic nerve terminal, voltage-gated calcium channels open, allowing Ca²⁺ influx - **Acetylcholine release** follows - the increased intracellular calcium causes synaptic vesicles containing acetylcholine to fuse with the presynaptic membrane and release the neurotransmitter into the synaptic cleft - **Sodium channels open in the end plate** last - acetylcholine binds to nicotinic receptors on the motor end plate, opening ligand-gated sodium channels, which depolarizes the muscle membrane and triggers muscle contraction *Incorrect: $1 \rightarrow 2 \rightarrow 3$* - Places sodium channel opening first, which is physiologically impossible - Sodium channels at the motor end plate only open in response to acetylcholine binding - Cannot occur before acetylcholine is released from the nerve terminal *Incorrect: $1 \rightarrow 3 \rightarrow 2$* - Incorrectly sequences sodium channel opening before calcium entry - Violates the fundamental principle that calcium influx is required for neurotransmitter release - Acetylcholine cannot be released without prior calcium entry *Incorrect: $3 \rightarrow 2 \rightarrow 1$* - Places acetylcholine release before calcium entry, which is impossible - Calcium-triggered exocytosis is an absolute requirement for neurotransmitter release - Without calcium influx, vesicles cannot fuse with the presynaptic membrane
Question 5: Which of the following is true about Lambert-Eaton syndrome?
- A. It is a paraneoplastic syndrome associated with squamous cell carcinoma of lung
- B. There is increase in release of presynaptic acetylcholine
- C. With continuous stimulation there is marked increase in amplitude of action potentials.
- D. IgG antibodies against voltage-gated calcium channels (Correct Answer)
Explanation: ***IgG antibodies against voltage-gated calcium channels*** - **Lambert-Eaton Myasthenic Syndrome (LEMS)** is an autoimmune disorder where **IgG antibodies** target **presynaptic voltage-gated calcium channels (VGCCs)** at the neuromuscular junction. - This antibody-mediated attack reduces the **calcium influx** into the presynaptic terminal, thereby impairing the release of **acetylcholine (ACh)**. *It is a paraneoplastic syndrome associated with squamous cell carcinoma of lung* - LEMS is most commonly associated with **small cell lung carcinoma (SCLC)**, constituting about 50-60% of cases as a **paraneoplastic syndrome** [1]. - While other cancers can be associated, **squamous cell carcinoma** is not the primary or most common lung cancer linked to LEMS. *There is increase in release of presynaptic acetylcholine* - In LEMS, the binding of autoantibodies to presynaptic **VGCCs** leads to a **reduction in calcium influx**, which in turn **decreases the release of acetylcholine** into the synaptic cleft. - This impairment of ACh release is the primary cause of muscle weakness characteristic of the syndrome [1]. *With continuous stimulation there is marked increase in amplitude of action potentials.* - A key electrophysiological feature of LEMS is a **pronounced increase in the compound muscle action potential (CMAP) amplitude** with repetitive nerve stimulation (e.g., 20-50 Hz) or after maximal voluntary contraction for 10-30 seconds. - However, the statement indicates a "marked increase in amplitude of action potentials" which is partially true but not completely accurate as it refers to the CMAP amplitude, rather than individual action potentials and "continuous stimulation" is more accurately described as high-frequency repetitive stimulation.
Question 6: Match the following: A) Glossopharyngeal nerve B) Spinal accessory nerve C) Facial nerve D) Mandibular nerve 1) Shrugging of shoulder 2) Touch sensation from the posterior one-third of the tongue 3) Chewing 4) Taste from the anterior two-thirds of the tongue
- A. A-3 , B-1 , C-4 , D-2
- B. A-2 , B-3 , C-4 , D-1
- C. A-4 , B-1 , C-2 , D-3
- D. A-2 , B-1 , C-4 , D-3 (Correct Answer)
Explanation: ***A-2 , B-1 , C-4 , D-3*** - **A) Glossopharyngeal nerve (CN IX)** is responsible for **general sensation and taste from the posterior one-third of the tongue** [1]. (2). - **B) Spinal Accessory nerve (CN XI)** innervates the **sternocleidomastoid** and **trapezius muscles**, which are involved in shrugging the shoulders (1). - **C) Facial nerve (CN VII)** carries **taste sensation from the anterior two-thirds of the tongue** [1] (4) via the chorda tympani. - **D) Mandibular nerve (V3)**, a branch of the trigeminal nerve, innervates the muscles of mastication, enabling **chewing** (3). *A-3 , B-1 , C-4 , D-2* - This option incorrectly associates the **glossopharyngeal nerve** with chewing, which is a function of the mandibular nerve (V3). - It also incorrectly associates the **mandibular nerve** with touch sensation from the posterior one-third of the tongue, which is a function of the glossopharyngeal nerve [1]. *A-2 , B-3 , C-4 , D-1* - This option incorrectly links the **spinal accessory nerve** with chewing; this nerve primarily controls shoulder and neck movements. - It also incorrectly assigns shrugging of the shoulder to the **mandibular nerve** instead of the spinal accessory nerve. *A-4 , B-1 , C-2 , D-3* - This choice incorrectly attributes **taste from the anterior two-thirds of the tongue** to the glossopharyngeal nerve, which supplies the posterior one-third [1]. - It also incorrectly links **touch sensation from the posterior one-third of the tongue** to the facial nerve, which is involved in taste from the anterior two-thirds [1].
Question 7: Primary afferent fibers secrete which nociceptive substance at the dorsal horn?
- A. Substance P (Correct Answer)
- B. Acetylcholine
- C. Norepinephrine
- D. Epinephrine
Explanation: ***Substance P*** - **Substance P** is a neuropeptide released by **C fibers** and **A-delta fibers** (primary afferent nociceptors) in the dorsal horn of the spinal cord. - It acts as a **neurotransmitter** and **neuromodulator**, contributing to the transmission and amplification of pain signals. *Acetylcholine* - **Acetylcholine** is a primary neurotransmitter in the **neuromuscular junction** and the autonomic nervous system. - While it has some roles in the CNS, it is not the primary nociceptive substance secreted by afferent fibers in the dorsal horn. *Norepinephrine* - **Norepinephrine** (noradrenaline) is a neurotransmitter involved in the **fight-or-flight response** and mood regulation. - It can modulate pain, but it is not directly released by primary afferent fibers as a nociceptive substance in the dorsal horn. *Epinephrine* - **Epinephrine** (adrenaline) is a hormone and neurotransmitter primarily associated with the **sympathetic nervous system** and stress response. - It does not serve as a direct nociceptive transmitter released by primary afferent fibers in the spinal cord.
Question 8: Which of the following is true regarding Lambert-Eaton myasthenic syndrome?
- A. Deep tendon reflexes are preserved
- B. Pyridostigmine can be used as treatment
- C. Associated with autoantibodies against P/Q-type calcium channels (Correct Answer)
- D. It is a presynaptic disorder of the neuromuscular junction that can cause weakness
Explanation: ***Associated with autoantibodies against P/Q-type calcium channels*** - **Lambert-Eaton Myasthenic Syndrome (LEMS)** is an **autoimmune disorder** where antibodies attack **presynaptic P/Q-type voltage-gated calcium channels** at the neuromuscular junction [1]. - This attack impairs the release of **acetylcholine**, leading to **muscle weakness**, particularly in the proximal limbs [2]. *Deep tendon reflexes are preserved* - In LEMS, **deep tendon reflexes are typically diminished or absent** at rest due to insufficient neurotransmitter release [2]. - Reflexes may transiently improve with **post-tetanic potentiation** after sustained muscle contraction [2]. *Pyridostigmine can be used as treatment* - **Pyridostigmine**, an **acetylcholinesterase inhibitor**, has limited efficacy in LEMS because the primary defect is in **acetylcholine release**, not its breakdown [1]. - While it may provide some mild benefit, it is **less effective** compared to its use in **myasthenia gravis** [1]. *It is a presynaptic disorder of the neuromuscular junction that can cause weakness* - While LEMS is indeed a **presynaptic disorder of the neuromuscular junction** that causes weakness, this statement is **less specific** than the correct option. - The most defining characteristic, which is specific to its pathophysiology, is the presence of **autoantibodies against P/Q-type calcium channels** [2].
Question 9: The mechanism of action of botulinum toxin A is best described by:
- A. Slowing of myelinated nerve fiber transmission
- B. Postsynaptic receptor blockade
- C. Acetylcholinesterase inhibition
- D. Presynaptic blockade of acetylcholine release (Correct Answer)
Explanation: ***Presynaptic blockade of acetylcholine release*** - **Botulinum toxin A** acts by cleaving specific proteins (**SNARE proteins** like SNAP-25, synaptobrevin, and syntaxin) essential for the fusion of **acetylcholine-containing vesicles** with the presynaptic membrane. - This prevents the release of acetylcholine into the **neuromuscular junction**, leading to muscle paralysis. *Slowing of myelinated nerve fiber transmission* - This describes the action of agents that affect **myelin sheaths** (e.g., demyelinating diseases) or ion channels involved in action potential propagation, not the mechanism of botulinum toxin. - Botulinum toxin specifically targets the **synaptic transmission**, not the speed of nerve conduction itself. *Postsynaptic receptor blockade* - This mechanism is seen with drugs like **curare** or **neuromuscular blockers** (e.g., rocuronium, vecuronium), which compete with acetylcholine for binding to **nicotinic acetylcholine receptors** on the muscle endplate. - Botulinum toxin does not affect the postsynaptic receptors directly; its action is entirely presynaptic. *Acetylcholinesterase inhibition* - **Acetylcholinesterase inhibitors** (e.g., neostigmine, pyridostigmine) prevent the breakdown of acetylcholine in the synaptic cleft, increasing its concentration and prolonging its action. - This mechanism would enhance, rather than block, muscle contraction, which is opposite to the effect of botulinum toxin.
Question 10: Retinal cells which secrete acetylcholine are:
- A. Bipolar cells
- B. Ganglion cells
- C. Amacrine cells (Correct Answer)
- D. Horizontal cells
Explanation: ***Amacrine cells*** - A subpopulation of **amacrine cells** in the retina is known to be **cholinergic**, meaning they synthesize and release **acetylcholine**. - These cholinergic amacrine cells play a role in **directional selectivity** and spatial processing within the retina. *Bipolar cells* - **Bipolar cells** primarily act as interneurons that transmit signals from photoreceptors to ganglion cells in the retina. - They typically release **glutamate** as their neurotransmitter, not acetylcholine. *Ganglion cells* - **Ganglion cells** are the output neurons of the retina, whose axons form the **optic nerve**. - While they receive input from cholinergic amacrine cells, ganglion cells themselves do not secrete acetylcholine; they are primarily glutamatergic. *Horizontal cells* - **Horizontal cells** are interneurons that provide lateral inhibition in the outer plexiform layer of the retina. - They primarily release **GABA** (gamma-aminobutyric acid) as their neurotransmitter, not acetylcholine.
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