Mu-type opioid receptor, Kappa-type opioid receptor, and Delta-type opioid receptor (MOR (mu-type opioid receptor), KOR (kappa-type opioid receptor), DOR (delta-type opioid receptor))

The mu-type, kappa-type, and delta-type opioid receptors are the three principal subtypes of classical opioid receptors, all of which belong to the G protein-coupled receptor (GPCR) family. These receptors mediate the effects of endogenous opioid peptides (such as endorphins, enkephalins, and dynorphins) as well as exogenous opioid drugs by coupling primarily to Gi/o proteins, which inhibit adenylate cyclase activity and modulate ion channels to reduce neuronal excitability[1][3][6]. - The mu opioid receptor (MOR) is the main mediator of most clinically relevant opioid effects including analgesia, euphoria, respiratory depression, miosis, and physical dependence[3][6][4]. - The kappa opioid receptor (KOR) primarily modulates spinal analgesia, diuresis, and dysphoria, and has roles in mood and the perception of pain and stress[3][4][5][6]. - The delta opioid receptor (DOR) is less well-studied but is implicated in mood regulation, modulation of pain (especially under inflammatory states), and gastrointestinal function[3][4][5][6]. Each receptor type has a distinct anatomical distribution within the central and peripheral nervous system and can form functional complexes or heterodimers, which may alter their pharmacological and physiological properties[1][2][6]. For clinical relevance, these receptors are the primary therapeutic targets for opioid analgesics, substances used in pain management, and for drugs addressing opioid dependence and overdose[3][4][6]. However, their chief therapeutic challenge lies in the high risk of tolerance, dependence, and significant side effects such as respiratory depression, constipation, and abuse potential, particularly with mu receptor agonists[3][4].

Other names

Mu opioid receptorKappa opioid receptorDelta opioid receptorμ-opioid receptorκ-opioid receptorδ-opioid receptorMORKORDOROP1 (mu)OP2 (kappa)OP3 (delta)

Agonism, Partial agonism, Antagonism, Biased agonism (G-protein coupling, beta-arrestin pathway modulation)