Molecular biology of the opioid receptors: structures, functions and distributions

Minami, Masabumi; Satoh, Masamichi

doi:10.1016/0168-0102(95)00933-k

Cited by 302 publications

(179 citation statements)

References 147 publications

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“…One possibility is that opioid receptors found on GABAergic terminals in CeA (originating in the intercalated cell masses) could regulate the inhibition of interneurons within the CeA. Since opioid receptors are linked to G-proteins that generally exert inhibitory control on the cell (for a review, see Minami and Satoh, 1995), microinjection of NAL into the CeA could enhance GABA release from intercalated terminals by relieving opioid receptor-mediated inhibition on these terminals. This enhanced GABA release would inhibit the interneurons of the CeA allowing for increased activity of projection neurons leaving the CeA.…”

Section: Discussionmentioning

confidence: 99%

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Burghardt

Wilson

2005

Neuropsychopharmacol

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The amygdala is involved in behavioral and physiological responses to fear, and the anxiolytic properties of several drugs are localized to this region. Activation of endogenous opioid systems is known to occur in response to stress and a growing body of literature suggests that opioid systems regulate the properties of anxiolytic drugs. These experiments sought to elucidate the role of opioid receptors in the central (CeA) and basolateral (BLA) nuclei of the amygdala in regulating the anxiolytic properties of ethanol and diazepam. Male rats fitted with cannula received bilateral microinjections of the nonselective opioid receptor antagonist naltrexone (NAL) immediately followed by systemic delivery of either ethanol (1 g/kg) or diazepam (2 mg/kg) in the elevated plus maze. Both diazepam and ethanol decreased anxiety-like behavior. Delivery of NAL into the CeA blocked the anxiolytic properties of diazepam. Delivery of NAL into the BLA slightly increased open arm avoidance, but had no effect on the anxiolytic properties of diazepam. Microinjection of NAL into either nucleus failed to block the effects of ethanol. These results were specific to the anxiolytic properties of diazepam, since baseline behaviors were unaffected by microinjection of NAL. Microinjection of lidocaine produced results distinct from NAL and failed to block the anxiolytic actions of diazepam. These studies indicate distinct roles for opioid receptor systems in the CeA and BLA in regulating the anxiolytic properties of diazepam in the elevated plus maze. Further, opioid receptor systems in the CeA and BLA do not regulate the anxiolytic properties of ethanol in this test.

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Section: Discussionmentioning

confidence: 99%

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Burghardt

Wilson

2005

Neuropsychopharmacol

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“…Three opioid receptor types, , ␦, and , are known, and they belong to the super family of G-protein-coupled receptors (Minami and Satoh, 1995;Law et al, 1999;Pasternak, 2004). Regulation of their expression has been extensively examined, primarily at the level of gene transcription regulated by vitamin A, cytokines (Bi et al, 2001;Park et al, 2002;Wei and Loh, 2002;Hu et al, 2004), and specific transcription factors (Kraus et al, 2001;Kim et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Tsai¹,

Bi²,

Loh³

et al. 2006

J. Neurosci.

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The expression of opioid receptor (KOR) is subjected to both transcriptional and posttranscriptional controls. We report that KOR translation is regulated by netrin-1 in primary neurons of dorsal root ganglion (DRG) and in P19 embryonal carcinoma cells. Without stimulation, a significant portion of KOR mRNA is maintained in a dormant state and partitions in the translationally inactive, postpolysomal fraction. During netrin-1 stimulation, which activates its downstream target focal adhesion kinase (FAK), KOR mRNA rapidly partitions to the translationally active polysomal fraction. Functionally, the newly synthesized KOR proteins in DRG neurons are able to bind to specific ligands. This report describes the first example of netrin-1 signaling in the translational control of a drug receptor KOR, which involves the mediator of netrin-1, FAK, and a novel mechanism that enhances the association of target mRNA with polysomes for translational activation.

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“…Finally, we have now shown that similarly to morphine the selective m-receptor agonist, DAMGO, when given intrastriatally decreases the release of DA in the striatum. This ®nding combined with the fact that the a nity of morphine for the cloned d-and k-opioid receptors is poor as compared with that for the m-opioid receptors (Fukuda et al, 1993;Minami & Satoh, 1995;Raynor et al, 1994) seems to rule out the involvement of d-and k-opioid receptors in this e ect of morphine.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Piepponen

Mikkola

Ruotsalainen

et al. 1999

British J Pharmacology

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1 The e ect of intrastriatally-administered morphine on striatal dopamine (DA) release was studied in freely moving rats. Morphine (1, 10 or 100 mM) was given into the striatum by reversed microdialysis, and concentrations of DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were simultaneously measured from the striatal dialysates. 2 Intrastriatally-administered morphine signi®cantly and dose-dependently decreased the extracellular concentration of DA, the concentrations of the acidic DA metabolites were only slightly decreased. The e ect of morphine was antagonized by naltrexone (2.25 mg kg 71 , s.c.). Pretreatment with a preferential k-opioid receptor antagonist, MR2266 [(7)-5,9 alpha-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphane; 1 mg kg 71 , s.c.], had no e ect on the decrease of extracellular DA evoked by intrastriatal morphine (100 mM). 3 Intrastriatal administration of the selective m-opioid receptor agonist [D-Ala 2 ,MePhe 4 ,Gly-ol 5 ] enkephalin (DAMGO; 1 mM), signi®cantly decreased the extracellular concentration of DA in the striatum. 4 When the rats were given morphine repeatedly in increasing doses (10 ± 25 mg kg 71 , s.c.) twice daily for 7 days and withdrawn for 48 h, the decrease of extracellular DA induced by morphine (100 mM) was signi®cantly less than that seen in saline-treated controls. 5 Our results show that besides the well-known stimulatory e ect there is a local inhibitory component in the action of morphine on striatal DA release in the terminal regions of nigrostriatal DA neurones. Tolerance develops to this inhibitory e ect during repeated morphine treatment. Furthermore, our results suggest that the e ect of intrastriatally-administered morphine is mediated by the m-opioid receptors.

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Molecular biology of the opioid receptors: structures, functions and distributions

Cited by 302 publications

References 147 publications

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

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