Central opioid receptor

The central opioid receptors encompass a family of G protein-coupled receptors—mu, delta, and kappa opioid receptors—expressed primarily in the CNS, where they mediate the effects of endogenous opioid peptides (endorphins, enkephalins, dynorphins) and exogenous opioids (morphine, fentanyl, etc.)[1][4][7][9]. These receptors play critical roles in pain modulation, reward, mood regulation, and various neurophysiological processes. The mu opioid receptor is the predominant target for clinical analgesics but also carries the risk of dependence, tolerance, and respiratory depression. Research into receptor structure and signaling has enabled the design of biased agonists aimed at dissociating therapeutic effects from adverse events[2][5]. The term "central opioid receptor" is not a specific molecular entity, and should be replaced in scientific contexts by reference to the explicit receptor subtype (MOR, DOR, KOR).

Other names

Mu receptorMOPMOPrOP3Delta receptorDOPrKappa receptorKOPrCentral opioid receptor (ambiguous, informal)

Agonism: Activation of MOR/DOR/KOR produces analgesia; MOR activation causes euphoria, DOR/KOR modulate mood and other effects Antagonism: Blocks opioid effects (e.g., naloxone reverses opioid overdose by MOR antagonism) Biased agonism: Selective pathway activation to minimize side effects (e.g., Gi-biased agonists for MOR)