Ad blocker interference detected!
Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers
Wikia is not accessible if you’ve made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected.
Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
- The title of this article should be Mu Opioid receptor. The initial letter is capitalized due to technical restrictions.
The μ opioid receptors (MOR) are a class of opioid receptors with high affinity for enkephalins and beta-endorphin but low affinity for dynorphins. The prototypical μ receptor agonist is the opium alkaloid morphine; μ (mu) refers to morphine.
They can exist either presynaptically or postsynaptically depending upon cell types.
The μ-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 μ-receptors 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.
μ receptors are also found in the intestinal tract. This causes constipation, a major side effect of μ agonists, due to inhibition of peristaltic action.
MOR can mediate acute changes in neuronal excitability via "disinhibition" of presynaptic release of GABA (see works from Charles Chavkin and Roger Nicoll). 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 (see works from Dezhi Liao and Horace Loh). 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 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 side effects, such as sedation, euphoria and decreased respiration, tend to lessen with continued use as tolerance develops. Analgesia, miosis and reduced bowel motility tend to persist; little tolerance develops to these effects.
Tolerance and overdosesEdit
Opioid overdoses kill through apnea and fatal hypoxia, often aggravated by simultaneous use of alcohol, benzodiazepines or barbiturates. However, substantial tolerance to respiratory depression develops quickly and tolerant individuals can easily withstand large doses fatal to opioid naïve individuals (an example of Mithridatism). Less commonly, massive overdoses have been known to cause circulatory collapse.
Tolerance to respiratory depression is lost just as quickly during withdrawal. Many, if not most fatal overdoses occur in addicts who take their usual doses after being in withdrawal long enough to lose their tolerance to respiratory depression.
Opioid overdoses can be rapidly reversed with any of several opioid antagonists: naloxone, or naltrexone, differing primarily in their duration of action and potency. While commonly referred to as antagonists, and when used to treat an overdose they do appear to function as such, naloxone & naltrexone are inverse agonists.
- ↑ Zhorov BS, Ananthanarayanan VS. Homology models of μ-opioid receptor with organic and inorganic cations at conserved aspartates in the second and third transmembrane domains. Arch Biochem Biophys. 37:31-49, 2000.
- ↑ Dortch-Carnes J, Russell K (2007). Morphine-stimulated nitric oxide release in rabbit aqueous humor. Exp. Eye Res. 84 (1): 185–90.
- ↑ Pan L, Xu J, Yu R, Xu MM, Pan YX, Pasternak GW (2005). Identification and characterization of six new alternatively spliced variants of the human mu opioid receptor gene, Oprm. Neuroscience. 133 (1): 209-20.
- ↑ Eisenberg RM (1994). TRIMU-5, a μ2-opioid receptor agonist, stimulates the hypothalamo-pituitary-adrenal axis. Pharmacol. Biochem. Behav. 47 (4): 943–6.
- ↑ Cadet P, Mantione KJ, Stefano GB (2003). Molecular identification and functional expression of μ3, a novel alternatively spliced variant of the human μ opiate receptor gene. J. Immunol. 170 (10): 5118–23.
- ↑ Stefano GB (2004). Endogenous morphine: a role in wellness medicine. Med. Sci. Monit. 10 (6): ED5.
- Opioid Receptors: μ. IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.
- MeSH mu+Opioid+Receptor
|Hypothalamic hormone receptors|
|Pituitary hormone receptors|
|Other hormone receptors|
|Other neuropeptide receptors|
|This page uses Creative Commons Licensed content from Wikipedia (view authors).|