opioidmediated

Opioid-mediated refers to processes or effects driven by opioids, including endogenous peptides such as endorphins, enkephalins, and dynorphins, as well as exogenous drugs like morphine, fentanyl, and oxycodone. These effects occur primarily through interactions with classical opioid receptors—mu (MOR), delta (DOR), kappa (KOR)—and the nociceptin receptor (NOP).

These receptors are G protein–coupled and their activation inhibits adenylyl cyclase, reduces cAMP, opens potassium channels, and closes calcium channels. This leads to decreased neuronal excitability and transmitter release. In the nervous system, opioid-mediated signaling modulates pain pathways at peripheral sites, within the spinal cord dorsal horn, and in supraspinal regions, as well as in reward and mood circuits of the limbic system.

Clinical and behavioral effects include analgesia, sedation, euphoria, cough suppression, respiratory depression, and miosis. Opioids also commonly cause constipation and, with chronic use, tolerance and physical dependence. Withdrawal can occur after cessation or antagonism. Opioid-induced hyperalgesia is a paradoxical increase in pain sensitivity that can accompany some opioid exposure. Individual responses can vary due to genetic factors affecting receptor signaling and metabolism.

In medical and research contexts, the term encompasses the mechanism of action of opioid analgesics and the role of endogenous opioids in pain, stress, and mood regulation. It also relates to adverse effects, risks of misuse and addiction, and the regulatory considerations surrounding opioid prescribing and safety.