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Pharmacology of Morphine
Morphine is a phenanthrene opioid receptor agonist – its main effect is binding to and activating the µ-opioid receptors in the central nervous system. Activation of these receptors is associated with analgesia, sedation, euphoria, physical dependence and respiratory depression. Morphine is known to bind very strongly to the µ-opioid receptors, hence its higher incidence of euphoria and dependence liability as compared to most other opioids. Morphine is also a κ-opioid and δ-opioid receptor agonist, κ-opioid's action is associated with spinal analgesia and miosis. δ-opioid is thought to play a role in analgesia. The effects of morphine can be countered with opioid antagonists such as naloxone, naltrexone and NMDA antagonists such as ketamine or dextromethorphan. Morphine is primarily metabolized into morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) via glucuronidation by phase II metabolism enzyme [UDP-glucuronosyl transferase-2B7] (UGT2B7). The phase I metabolism cytochrome P450 (CYP) family of enzymes has a role in the metabolism to a lesser extent. The metabolism occurs not only in the liver, but may also take place in the brain and the kidneys. M6G has been found to be a far more potent analgesic than morphine when dosed to rodents but crosses the blood-brain barrier with difficulty. M6G has been shown to be relatively more selective for mu-receptors than for delta- and kappa-receptors while M3G does not appear to compete for opioid receptor binding. The significance of M6G formation on the observed effect of a dose of morphine is the subject of extensive debate among pharmacologists.

Related Topics

Introduction to Morphine		Pharmacology of Morphine
History of Morphine
Opium		Heroin

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