## Opioid Receptor Subtypes and Their Functions **Key Point:** The μ (mu) receptor is the primary opioid receptor responsible for both the therapeutic analgesic effects and the major adverse effects (respiratory depression, physical dependence) of opioids. ### Receptor Classification and Effects | Receptor | Primary Effects | Clinical Significance | |----------|-----------------|----------------------| | **μ (mu)** | Analgesia, respiratory depression, euphoria, physical dependence | Mediates both therapeutic and adverse effects | | **δ (delta)** | Analgesia (minor), dysphoria, seizures | Minimal clinical relevance; mainly research | | **κ (kappa)** | Analgesia, dysphoria, diuresis, no respiratory depression | Spinal analgesia; less abuse potential | | **σ (sigma)** | Dysphoria, hallucinations, psychotomimetic effects | Not a true opioid receptor; blocked by naloxone | ### Mechanism of μ Receptor Action **High-Yield:** μ receptors are G-protein coupled receptors (GPCRs) that: 1. Decrease cAMP levels via Gi/o protein coupling 2. Increase K^+^ efflux (hyperpolarization) 3. Decrease Ca^2+^ influx (reduced neurotransmitter release) 4. Result: decreased pain signal transmission in spinal cord and brainstem **Clinical Pearl:** All clinically used opioids (morphine, codeine, fentanyl, tramadol) exert their primary analgesic action through μ receptor agonism. Respiratory depression—the dose-limiting adverse effect—is also μ-mediated, occurring at the chemoreceptor trigger zone and respiratory centers in the medulla. **Warning:** σ (sigma) receptors are NOT true opioid receptors and are NOT blocked by naloxone antagonism, despite historical classification. They are now recognized as distinct from the opioid receptor family.
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