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Opioid receptors
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	NOP

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μ

Previous and Unofficial Names OP3 MOR MOR-1 Structural Information class A G protein-coupled receptor Species TM AA Chromosomal Location Gene Name Reference Human 7 400 6q24-q25 OPRM1 153 Rat 7 398 1p11 Oprm1 148-152 Mouse 7 398 10 A2 Oprm1 154

Contents: Previous and Unofficial Names Structural Information Database Links Agonists Antagonists Allosteric Regulators Transduction Mechanisms Tissue Distribution Functional Assays Physiological Functions Physiological Consequences of Altering Gene Expression Biologically Significant Variants

Database Links
ChEMBL Target	129 (Hs), 12471 (Mm), 10529 (Rn)
Ensembl	ENSG00000112038 (Hs), ENSMUSG00000000766 (Mm)
Entrez Gene	4988 (Hs), 18390 (Mm), 25601 (Rn)
GeneCards	OPRM1 (Hs)
HomoloGene	37368 (Hs)
OMIM	600018 (Hs)
Protein Ontology (PRO)	PRO:000001612 (Hs)
RefSeq Nucleotide	NM_000914 (Hs), NM_001039652 (Mm), NM_013071 (Rn)
RefSeq Protein	NP_000905 (Hs), NP_001034741 (Mm), NP_037203 (Rn)
UniGene Hs.	2353 (Hs)
UniProt	P35372 (Hs), P42866 (Mm), P33535 (Rn)
Wikipedia	μ

Search for 3D structures on the PDB
Search using keywords: Opioid receptors mu	Search using accession numbers: P33535 || P35372 || P42866

Agonists
Key to terms and symbols	View all chemical structures	Click column headers to sort
Ligand Sp. Action Affinity Units Reference [tyrosyl 3,5-3H]DAMGO Rn Full agonist 8.7 pKd 56 (-)-cyclazocine Hs Partial agonist 10.0 pKi 12 etonitazene Hs Full agonist 9.7 pKi 12 (-)-EKC Hs Full agonist 9.5 pKi 12 etorphine Hs Full agonist 9.5 pKi 12 fentanyl Rn Full agonist 9.4 pKi 56 DAMGO Hs Full agonist 9.3 pKi 12 fentanyl Hs Full agonist 9.2 pKi 12 [Met]-enkephalin Rn Full agonist 9.2 pKi 56 (-)-methadone Hs Full agonist 9.2 pKi 12 β endorphin Rn Full agonist 9.0 pKi 56 morphine Hs Full agonist 9.0 pKi 12 buprenorphine Hs Partial agonist 8.8 pKi 12 dihydromorphine Hs Full agonist 8.8 pKi 12 dynorphin 1-11 Hs Full agonist 8.8 pKi 12 normorphine Hs Full agonist 8.8 pKi 12 DADLE Hs Full agonist 8.7 pKi 12 DAMGO Rn Full agonist 8.7 pKi 56 dynorphin B Hs Full agonist 8.5 pKi 12 dynorphin 1-8 Hs Full agonist 8.4 pKi 12 (-)-pentazocine Hs Partial agonist 8.4 pKi 12 dynorphin 1-13 Hs Full agonist 8.3 pKi 12 endomorphin-1 {Sp: Human} Hs Full agonist 8.3 pKi 58 DSLET Hs Full agonist 8.2 pKi 12 PL017 Hs Full agonist 8.2 pKi 12 dynorphin 1-17 Hs Full agonist 8.1 pKi 12 [Leu]-enkephalin Hs Partial agonist 8.1 pKi 12 morphine Rn Partial agonist 7.9 pKi 56 codeine Hs Full agonist 6.9 pKi 12
View species-specific agonist tables
Agonist Comments
pKi values were determined in the absence of Na+ and guanine nucleotides. Discrimination of full or partial agonism is very dependent on the level of receptor expression and on the assay used to monitor agonist effects. Many agents may behave as full agonists or potent partial agonists in cell lines expressing cloned receptors in high concentration, but in other environments they may show only weak agonist activity. The identification of agonist activity in the table is largely based on the ability to stimulate GTPγ35S binding in cell lines expressing cloned human mu receptors. Agents giving 85% or greater stimulation than that given by DAMGO have been characterized as Full Agonists [12]. It is still unclear whether endomorphins are endogenous. Morphine occurs endogenously [158].

Antagonists
Key to terms and symbols	View all chemical structures	Click column headers to sort
Ligand Sp. Action Affinity Units Reference [3H]diprenorphine Mm Antagonist 10.1 pKd 56 [N-allyl-2,3-3H]naloxone Mm Antagonist 9.0 pKd 56 naloxonazine Mm Antagonist 10.3 pKi 56 diprenorphine Mm Antagonist 10.1 pKi 56 (-)-quadazocine Hs Antagonist 10.0 pKi 12 (-)-bremazocine Hs Antagonist 9.7 pKi 12 CTOP Hs Antagonist 9.7 pKi 56 naltrexone Hs Antagonist 9.7 pKi 12 β-FNA Hs Antagonist 9.5 pKi 12 β-FNA Mm Antagonist 9.5 pKi 56 nalmefene Hs Antagonist 9.5 pKi 12 diprenorphine Hs Antagonist 9.1 pKi 12 naloxone Mm Antagonist 9.0 pKi 56 nalorphine Hs Antagonist 8.9 pKi 12 naloxone Hs Antagonist 8.9 pKi 12 BNTX Hs Antagonist 8.8 pKi 12 naloxone benzoylhydrazone Hs Antagonist 8.7 pKi 12 CTAP Hs Antagonist 8.6 pKi 12 naloxone benzoylhydrazone Hs Antagonist 8.2 pKi 12 naltrindole Hs Antagonist 8.2 pKi 12 naltriben Hs Antagonist 7.9 pKi 12 nor-binaltorphimine Hs Antagonist 7.7 pKi 12
View species-specific antagonist tables
Antagonist Comments
β-FNA is an electrophilic affinity label. The pKi reflects both the reversible and irreversible binding components. CTOP is a good somatostatin receptor (sst receptor) agonist in addition to having antagonist activity at μ opioid receptors; it should never be used in studies of μ receptor function in situations where sst receptors may be involved. CTAP does not activate sst receptors [159].

Allosteric Regulator Comments

Although no small molecules are considered direct allosteric regulators of μ receptors, a number of proteins such as G protein-coupled receptor kinases, β-arrestins and G proteins clearly regulate μ opioid receptor affinities and function. Furthermore sodium and guanyl nucleotides can modify the functional μ receptor complex and G protein interaction. Also, μ receptors are reported to form heterodimers with other receptors of the OP family or with non-opioid G protein-coupled receptors. Heterodimerisation may alter μ receptor function and/or trafficking [155-157].

Primary Transduction Mechanisms
Transducer	Effector/Response
Gi/Go family	Adenylate cyclase stimulation Adenylate cyclase inhibition Phospholipase C stimulation Potassium channel Calcium channel Phospholipase A2 stimulation Phospholipase D stimulation Other - See Comments
Comments:  The following systems have also been reported to be activated following Gi/Go activation via the μ receptor: epidermal growth factor receptor transactivation and subsequent mitogen activated protein kinase ERK [160-161], Jun N-terminal kinase (JNK) expression and activity [162-164], signal transducer and activator of transcription 3 (STAT3) [165], focal adhesion kinase [166], nuclear Ca2+/calmodulin translocation [167], phosphatidylinositol-3 kinase expression and activity [162,168].
References:  87-88,169-183

Secondary Transduction Mechanisms
Transducer	Effector/Response
Gq/G11 family	Phospholipase C stimulation
Comments:  G16 couples to the μ opioid receptor and activates PLC.
References:  89,184

Tissue Distribution
Accessory optic tract. Species:  Rat Technique:  Immunohistochemistry. References:  240
CNS: superficial layers of the medullary and spinal dorsal horns. Colocalisation with substance P. Species:  Rat Technique:  immunocytochemistry. References:  241-242
CNS: thalamus, striatum, hypothalamus and pons-medulla > hippocampus and midbrain > cerebral cortex and cerebellum. Species:  Rat Technique:  Northern blotting. References:  256
CNS: superficial layers (laminae I and II) of the dorsal horn of the spinal cord. Species:  Rat Technique:  Radioligand binding. References:  49
Pregnant uterus. Species:  Mouse Technique:  in situ hybridisation. References:  45
CNS: anterior cingulate cortex, neocortex, amygdala, hippocampus, ventral dentate gyrus, presubiculum, nucleus accumbens, caudate putamen, thalamus, habenula, interpeduncular nucleus, pars compacta of the substantia nigra, superior and inferior colliculi, raphe nuclei. Species:  Rat Technique:  Radioligand binding. References:  97
CNS: Olfactory bulb, striatal patches and subcallosal streak, medial septum, piriform and cingulate cortex, entorhinal cortex, bed nucleus stria terminalis, medial preoptic area, globus and ventral pallidum, thalamic nuclei, lateral hypothalamus, mammillary nuclei , hippocampus, amygdaloid nuclei, ventral and lateral periaqueductal grey, ventral tegmental area and substantia nigra pars compacta, superior and inferior colliculi, interpeduncular nuclei, locus ceruleus, parabrachial nuclei, median raphe, nucleus of the solitary tract, spinal cord (dorsal root ganglia and layers I and II). Species:  Rat Technique:  in situ hybridisation. References:  150
CNS: olfactory bulb. Species:  Rat Technique:  immunocytochemistry. References:  224
CNS: cerebral cortex, striatum, hippocampus, locus coeruleus, superficial laminae of the dorsal horn. Species:  Rat Technique:  Immunohistochemistry. References:  234
Gastrointestinal tract. Species:  Rat Technique:  Immunohistochemistry. References:  235
CNS: superficial layers of the dorsal horn. Species:  Rat Technique:  immunocytochemistry. References:  236-237
Immune cells: CEM x174 T/B lymphocytes, Raji B cells, CD4+, monocytes/macrophages, neutrophils. Species:  Human Technique:  RT-PCR. References:  238
CNS: striatum, medial habenular nucleus, medial terminal nucleus of the accessory optic tract, interpeduncular nucleus, median raphe nucleus, parabrachial nuclei, locus coeruleus, ambiguous nucleus, nucleus of the solitary tract, and laminae I and II of the medullary and spinal dorsal horns, cerebral cortex, amygdala, thalamus, and hypothalamus. Species:  Rat Technique:  Immunohistochemistry. References:  239
CNS: striatum, layers I and III of the cortex, the pyramidal cell layer of the hippocampal formation, specific nuclei of the thalamus, the pars reticulata of the substantia nigra, the interpeduncular nucleus, and the locus coeruleus. Species:  Rat Technique:  Radioligand binding. References:  101
CNS: caudate putamen. Species:  Rat Technique:  immunocytochemistry. References:  243-244
CNS: superficial layers of the spinal cord dorsal horn, nucleus caudalis of the spinal tract of the trigeminal, nucleus of the solitary tract, nucleus ambiguous, locus coeruleus, interpeduncular nucleus, lateral habenular nucleus, caudate-putamen, nucleus accumbens, ventral tegmental area, thalamus, hypothalamus, amygdaloid nuclei, nucleus accumbens, cerebral cortex, septum and diagonal band, preoptic area, medial thalamic and habenular nuclei, locus coeruleus, nucleus ambiguous, trigeminal nucleus caudalis, spinal cord substantia gelatinosa zones. Species:  Rat Technique:  Immunohistochemistry. References:  245
CNS: Purkinje cells and granular and molecular layers of the fetal, neonatal and adult cerebellum. Species:  Rat Technique:  Immunohistochemistry. References:  246
Ear: cochleae. Species:  Rat Technique:  RT-PCR. References:  43,247
Skin: dermal and epidermal nerve fibers. Species:  Human Technique:  Immunohistochemistry. References:  248
CNS: nucleus accumbens (plasma membranes: extrasynaptic neuronal > glial) Species:  Rat Technique:  immunocytochemistry. References:  249
CNS: nucleus accumbens (plasma membranes of GABAergic neurons). Species:  Rat Technique:  immunocytochemistry. References:  250
CNS: locus coeruleus (noradrenergic perikarya and dendrites). Species:  Rat Technique:  immunocytochemistry. References:  251-252
CNS: accessory olfactory bulb, striatal patches and streaks, amygdaloid nuclei, ventral hippocampal subiculum and dentate gyrus, numerous thalamic nuclei, geniculate bodies, central grey, superior and inferior colliculi, solitary and pontine nuclei and substantia nigra. Species:  Rat Technique:  Radioligand binding. References:  253
CNS: thalamus, striosomes of the caudate-putamen, globus pallidus, cerebral cortex. Species:  Rat Technique:  in situ hybridisation. References:  254
CNS: thalamic, brainstem and reticular core nuclei (highest in the habenular and thalamic nuclei). Species:  Rat Technique:  in situ hybridisation. References:  99
CNS: accessory olfactory bulb, anterior olfactory nuclei, striatal patches of the nucleus accumbens and caudate-putamen, endopiriform nucleus, claustrum, diagonal band of Broca, globus pallidus, ventral pallidum, bed nucleus of stria terminalis, most thalamic nuclei, medial and posteriocortical medial amygdala, lateral, dorsomedial, posterior and mammillary nuclei of the hypothalamus, presubiculum, subiculum, rostral interpeduncular nucleus, median raphe, inferior colliculus, parabrachial nucleus, locus coeruleus, central grey, nucleus ambiguus, nucleus of the solitary tract, nucleus gracilis, nucleus cuneatus, dorsal motor nucleus of vagus. Species:  Rat Technique:  In situ hybridisation and radioligand binding. References:  255
CNS: olfactory bulb, caudate-putamen, nucleus accumbens, lateral and medial septum, diagonal band of Broca, bed nucleus of the stria terminalis, most thalamic nuclei, hippocampus, amygdala, medial preoptic area, superior and inferior colliculi, central gray, dorsal and median raphe, raphe magnus, locus coeruleus, parabrachial nucleus, pontine and medullary reticular nuclei, nucleus ambiguus, nucleus of the solitary tract, nucleus gracilis and cuneatus, dorsal motor nucleus of vagus, spinal cord, dorsal root ganglia. Species:  Rat Technique:  in situ hybridisation. References:  257
CNS: caudate putamen, nucleus accumbens, endopiriform nucleus, fundus striati, habenula, amygdaloid nuclei, thalamus, hypothalamus, zona incerta, ventral tegmental area, interpeduncular nucleus, central gray, dentate gyrus, substantia nigra, the superior colliculus. Species:  Mouse Technique:  Radioligand binding. References:  46
Tissue Distribution Comments
μ opioid receptors are widely distributed with dense labelling throughout the fore, mid and hindbrain regions in the CNS. Quantitatively, the μ receptor is the most highly expressed of all the opioid receptors. Although the early studies used non-selective ligands such as [3H]dihydromorphine, characterisation of the distribution of the μ opioid receptor has been aided by the availability of [3H]DAMGO, a highly selective opioid agonist that has been the ligand of choice for labelling μ opioid receptors for over 20 years. Immunohistochemistry has largely confirmed receptor autoradiography. For a review of μ opioid receptor expression in the rat see [23].

Functional Assays
Measurement of intracellular cAMP levels in SH-SY5Y cells endogenously expressing the μ receptor. Species:  Human Tissue:  SH-SY5Y cells. Response measured:  Inhibition of cAMP accumulation. References:  233
Measurement of [35S]GTPγS binding. Species:  Rat Tissue:  Brain slices. Response measured:  [35S]GTPγS binding. References:  1

Physiological Functions
Constriction of the pupil. Species:  Human Tissue:  Pupil. References:  258
DAMGO increases the conductance of an inwardly rectifying potassium conductance and hyperpolarises locus coeruleus neurons. Species:  Rat Tissue:  Brain. References:  179
μ receptor agonsts reduce bith early (GABAA receptor-mediated) and late (GABAB receptor-mediated) inhibitory postsynaptic currents in the dentate gyrus of hippocampal slices. Species:  Rat Tissue:  Hippocampal slices. References:  259
Morphine inhibits N- and P/Q-type Ca2+ channels in the nucleus traxtus solitarius of the rat. Species:  Rat Tissue:  Brain. References:  182
Morphine is responsible for modulating the Ca2+ currents in the mouse periaqueductal grey neurons. Species:  Mouse Tissue:  Periaqueductal grey neurons. References:  174
Morphine inhibits interpheron (IFN)-γ promotor activity in activated mouse T cells, which is mediated through two distinct cAMP-dependent pathways, the NF-κB signalling pathway and the ERK1/2, p38 MAPK, AP-1/NFAT pathway. Species:  Mouse Tissue:  T cells. References:  260
Body temperature regulation: μ receptor activation induces hypothermia, blocked by selective μ receptor antagonists. The effect is centrally mediated, involving both oxidative metabolism and heat exchange. Species:  Rat Tissue:  In vivo. References:  129

Physiological Consequences of Altering Gene Expression
Analgesia: Untreated μ receptor knockout mice display shorter latencies on tail flick and hot plate tests for spinal and supraspinal nociceptive responses than wild-type mice, which support the role for endogenous opioid-peptide interactions with the μ receptor in normal nociceptive processing. Interestingly, analgesia produced by the δ opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) in hot plate and tail flick tests is dramatically reduced in μ opioid receptor knockout mice in a gene-dose-dependent fashion, suggesting that DPDPE may require μ opioid receptor occupancies for full efficacy. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  14,185-188
Analgesia: Loss of μ opioid receptors prevents the plasma membrane translocation of δ opioid receptors in the dorsal horn of the spinal cord caused by chronic inflammatory pain induced by intraplantar injection of Freund's adjuvant. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  189-190
Addictions; drug-induced reinforcement: Opioid self-administration is abolished in μ receptor knockout mice. On the contrary, morphine is aversive in the μ opioid deficient mice by interaction with κ opioid receptors. In addition, μ opioid receptors may play a role in mediating various addictive agents such as ethanol, cocaine, nicotine and cannabinoid. Ethanol consumption is decreased in μ opioid knockout mice, and the animals exhibit less ethanol reward in a conditioned place preference paradigm. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  191-198
Addictions; locomotor activity: Cocaine-induced locomotor activity but not sensitisation is abolished in μ receptor knockout mice, while wild-type and heterozygous μ receptor mice display reduced cocaine conditioned place-preference, confirming a central role of μ receptors in drug reward but opposing effects in locomotor sensitisation. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  199
Emotional responsivity: μ opioid receptors may play a role in the modification of emotional responses to novelty, anxiety and depression. μ receptor knockout mice show less anxiety in the elevated plus maze and emergence tests, reduced response to novel stimuli in the novelty test and less depressive-like behaviour in the forced swim test. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  28
Attachment behaviour: Pups of μ receptor knockout mice emit fewer ultrasonic vocalisations when removed from their mothers. It indicates a role for μ opioid receptors in diseases characterised by deficits in attachment behaviour, such as autism or reactive attachment disorder. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  200
Modulation of neurotransmitter systems, dopamine: Administration of apomorphine increases the locomotor activity of μ receptor knockout mice more than wild-type mice, which may be related to the increased binding sites of the dopamine D2 receptor in the caudate putamen of receptor deficient mice. A tonically active μ opioid system modulates the basal dopamine neurotransmission in the nucleus accumbens (NAc). Microdialysis studies have revealed significant decreases in the dopamine fraction in μ opioid receptor knckout mice. μ opioid receptor knockout mice show diminished food-anticipatory activity which is dependent on μ-regulated dopaminergic activity. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  201-202
Modulation of neurotransmitter systems, acetylcholine: Muscarinic M1 receptor mRNA and protein levels are reduced in various bran regions when compared to the wild-type. In μ opioid receptor deficient mice an up-regulation of acetylcholinesterase activity and compensatory down-regulation of M2 muscarinic receptors in the striatal caudate putamen and nucleus accumbens have been reported, which can be associated with the enhanced tremors after administration of acetylcholinesterase inhibitors. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  203
Modulation of neurotransmitter systems, glutamate, somatostatin: An increase in glutamate and somatostatin binding was observed in μ receptor knockout mice, which may contribute to the enhanced excitability in these mice, showing an accelerated kindling development induced by the convulsant drug pentylenetetrazol. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  200
Learning and memory: Several studies have demonstrated that the loss of μ opioid receptors decreases LTP in the dentate gyrus of the hippocampus, suggesting the possibility that the lack of μ opioid receptors may acccompany a change in learning and memory. μ opioid receptor knockout mice show a significant spatial memory impairment compared to wild-type in the Morris water maze. They also exhibit an impairment in the ultimate level of spatial learning, suggesting that the μ opioid receptor may play a positive role in learning and memory by increasing LTP in CA3 neurons. On the other hand, the learning deficit induced in pentylenetetrazol kindling id absent in μ opioid receptor knockout mice. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  204-206
Immune responses: In μ receptor knockout mice chronic morphine administration cannot induce lymphoid organ atrophy, nor diminish the ratio of CD4+ CD8+ cells in the thymus nor reduce natural killer activity. Morphine modulation of macrophage phagocytosis and macrophage secretion of TNFα is not observed in μ receptor knockout animals. In contrast, morphine reduction of splenic and thymic cell number and mitogen-induced proliferation are unaffected, as is morphine inhibition of Il-1 and Il-6 secretion by macrophages. Morphine treatment promotes T(H2) differentiation through a μ opioid dependent mechanism. Developing T cells are responsive to the chemotactic effect of μ opioid agonists, an effect not seen in μ opioid knockout mice. Deficiency of μ receptor exacerbates experimental colitis whereas administration of the μ receptor agonist DAMGO reduces inflammation in wild-type mice. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  207-211
Other physiological functions: Sexual function in male homozygotes is affected, as shown by reducing mating activity and a decrease in sperm count and motility. Morphine-induced inhibition of gastrointestinal transit is abolished in μ receptor knockout mice, and basal GI motility is lower as compared to heterozygous and wild-type animals. μ opioid receptor knockout mice develop insulin resistance more rapidly than wild-type mice indicating a role for μ in controlling insulin resistance. Species:  Mouse Tissue:  Technique:  Gene targeting in embryonic stem cells. References:  212-213

Biologically Significant Variants
Several splice variant forms of the μ receptor (formerly MOR-1) have been identified. These variant forms were designated MOR-1A through MOR-1X; some of the variants express truncated forms of the receptor. The B, C and D variants differ in the amino acid composition at the C-terminus. The distribution of the protein expressed from the B, C and D variant forms has been studied by immunohistochemistry in the rat brain. They show a different distribution in the brain and spinal cord. When compared to the μ receptor, MOR-1D is deferentially desensitised in response to opioid agonists. Type:  Splice variants. Species:  Mouse References:  176,214-226
An Asn40 -> Asp polymorphism has been found in high abundance in the caucasian and asian population. There are studies showing functional differences of the variant to wild-type receptor in vitro and in vivo. In addition, there are several reports showing association of this polymorphism with addiction and idiopathic epilepsy. Type:  Single nucleotide polymorphism. Species:  Human References:  227-231
A rare Ser268 -> Pro polymorphism has been identified in the human receptor gene. The variant receptor possesses a marked reduction in coupling efficiency and is less desensitised upon agonist exposure. Type:  Single nucleotide polymorphism. Species:  Human References:  232
Biologically Significant Variant Comments
There are many additional polymorphisms of the μ receptor which are either without function or their functional significance is presently unknown.

To cite this receptor data page, please use the following:

Anna Borsodi, Girolamo Caló, Charles Chavkin, MacDonald J. Christie, Olivier Civelli, Brian M. Cox, Lakshmi A. Devi, Christopher Evans, Volker Höllt, Graeme Henderson, Brigitte Kieffer, Ian Kitchen, Mary-Jeanne Kreek, Lee-Yuan Liu-Chen, Jean-Claude Meunier, Philip S. Portoghese, Toni S. Shippenberg, Eric J. Simon, Lawrence Toll, John R. Traynor, Hiroshi Ueda, Yung H. Wong.
Opioid receptors: μ. Last modified on 2010-06-30. Accessed on 2010-09-03. IUPHAR database (IUPHAR-DB), http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=319.

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