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Academic Rationale:

Acetylcholine (ACh) is the sole neurotransmitter released at the somatic neuromuscular junction. It binds to nicotinic (N2) receptors on skeletal muscle, causing depolarization and muscle contraction. Norepinephrine is released at sympathetic neuroeffector junctions, not NMJ.

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Academic Rationale:

Atropine is a competitive muscarinic antagonist. In the eye, blocking M3 receptors on sphincter pupillae causes unopposed sympathetic action → mydriasis. Blocking ciliary muscle M3 receptors causes cycloplegia (loss of accommodation). R correctly explains the mechanism.

Correct Answer Node:

Academic Rationale:

Pilocarpine (muscarinic agonist) causes miosis and increases aqueous humor outflow → used in glaucoma (b). Neostigmine (AChE inhibitor) increases ACh at NMJ → reverses non-depolarizing muscle relaxants (a). Ipratropium (inhaled muscarinic antagonist) causes bronchodilation in COPD/asthma (c).

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Academic Rationale:

Atenolol is a cardioselective β1-blocker with minimal β2 effects at therapeutic doses. Propranolol is non-selective (β1+β2). Prazosin is an α1-blocker. Labetalol has both α and β blocking activity.

Correct Answer Node:

Academic Rationale:

α1 receptors couple to Gq → IP3/DAG → Ca2+ release → smooth muscle contraction (vasoconstriction) (I). β2 receptors couple to Gs → ↑cAMP → smooth muscle relaxation (bronchodilation) (II). Presynaptic α2 receptors are autoreceptors that inhibit NE release via negative feedback (III). All correct.