Morphine produces analgesia primarily through which receptor and intracellular mechanism?
- A κ (kappa) opioid receptors coupled to Gs proteins → increased cAMP and excitatory neurotransmission
- B μ (mu) opioid receptors coupled to Gi proteins → decreased cAMP, increased K+ conductance (hyperpolarisation), decreased Ca2+ influx ✓
- C δ (delta) opioid receptors coupled to Gq proteins → PLC activation and PKC-mediated analgesia
- D NMDA receptor antagonism, similar to ketamine
Explanation
Morphine's analgesia is mediated primarily through mu (μ) opioid receptors, which are Gi/Go-protein coupled. Gi activation inhibits adenylyl cyclase, reducing cAMP; additionally, it increases inwardly rectifying K+ channel conductance (hyperpolarisation) and reduces voltage-gated Ca2+ channel activity at presynaptic terminals. Together, these reduce neuronal excitability and neurotransmitter release in pain pathways. Mu receptors also mediate euphoria, respiratory depression, and constipation.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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