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μ-opioid receptor

μ-opioid receptor

The μ-opioid receptors (MOR) are a class of opioid receptors with a high affinity for enkephalins and beta-endorphin, but a low affinity for dynorphins. They are also referred to as μ-opioid peptide (MOP) receptors. The prototypical μ-opioid receptor agonist is morphine, the primary psychoactive alkaloid in opium. It is an inhibitory G-protein coupled receptor that activates the Gi alpha subunit, inhibiting adenylate cyclase activity, lowering cAMP levels.

, LMOR, M-OR-1, MOP, MOR, MOR1, OPRM, opioid receptor mu 1
External IDs
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)


Three variants of the μ-opioid receptor are well characterized, though RT-PCR has identified up to 10 total splice variants in humans. [666666] [undefined]

μ 1More is known about the μ1opioid receptor than the other variants.
μ 2TRIMU 5is a selective agonist of the μ2receptor.[undefined]
μ 3The μ3variant was first described in 2003.[undefined]It is responsive to opiatealkaloidsbut notopioid peptides.[undefined]


They can exist either presynaptically or postsynaptically depending upon cell types.

The μ-opioid receptors exist mostly presynaptically in the periaqueductal gray region, and in the superficial dorsal horn of the spinal cord (specifically the substantia gelatinosa of Rolando). Other areas where they have been located include the external plexiform layer of the olfactory bulb, the nucleus accumbens, in several layers of the cerebral cortex, and in some of the nuclei of the amygdala, as well as the nucleus of the solitary tract.

Some MORs are also found in the intestinal tract.

Activation of these receptors inhibits peristaltic action which causes constipation, a major side effect of μ agonists.



MOR can mediate acute changes in neuronal excitability via suppression of presynaptic release of GABA. Activation of the MOR leads to different effects on dendritic spines depending upon the agonist, and may be an example of functional selectivity at the μ-receptor. [undefined] The physiological and pathological roles of these two distinct mechanisms remain to be clarified. Perhaps, both might be involved in opioid addiction and opioid-induced deficits in cognition.

Activation of the μ-opioid receptor by an agonist such as morphine causes analgesia, sedation, slightly reduced blood pressure, itching, nausea, euphoria, decreased respiration, miosis (constricted pupils), and decreased bowel motility often leading to constipation. Some of these effects, such as analgesia, sedation, euphoria, itching and decreased respiration, tend to lessen with continued use as tolerance develops. Miosis and reduced bowel motility tend to persist; little tolerance develops to these effects.

The canonical MOR1 isoform is responsible for morphine-induced analgesia, whereas the alternatively spliced MOR1D isoform (through heterodimerization with the gastrin-releasing peptide receptor) is required for morphine-induced itching. [666666]


As with other G protein-coupled receptors, signalling by the μ-opioid receptor is terminated through several different mechanisms, which are upregulated with chronic use, leading to rapid tachyphylaxis. [undefined] The most important regulatory proteins for the MOR are the β-arrestins arrestin beta 1 and arrestin beta 2, [undefined] [undefined] [undefined] and the RGS proteins RGS4, RGS9-2, RGS14, and RGSZ2. [undefined] [undefined]

Long-term or high-dose use of opioids may also lead to additional mechanisms of tolerance becoming involved.

This includes downregulation of MOR gene expression, so the number of receptors presented on the cell surface is actually reduced, as opposed to the more short-term desensitisation induced by β-arrestins or RGS proteins.

[666666] [undefined] [undefined] Another long-term adaptation to opioid use can be upregulation of glutamate and other pathways in the brain which can exert an opioid-opposing effect, so reduce the effects of opioid drugs by altering downstream pathways, regardless of MOR activation. [undefined] [undefined]

Tolerance and overdoses

Fatal opioid overdose typically occurs due to bradypnea, hypoxemia, and decreased cardiac output (hypotension occurs due to vasodilation, & bradycardia further contributes to decreased cardiac output). [undefined] [666666] [undefined] A potentiation effect occurs when opioids are combined with ethanol, benzodiazepines, or barbiturates, which results in an increased risk for overdose to occur. [undefined] [666666] Substantial tolerance to respiratory depression develops quickly, and tolerant individuals can withstand larger doses. [666666] However, tolerance to respiratory depression is lost just as quickly during withdrawal. [666666] Many overdoses occur in people who misuse their medication after being in withdrawal long enough to lose the tolerance to respiratory depression. Less commonly, massive overdoses have been known to cause circulatory collapse.

Opioid overdoses can be rapidly reversed through the use of opioid antagonists, naloxone being the most widely used example. [undefined]

See also

  • δ-opioid receptor

  • κ-opioid receptor


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