Tissue distribution of the opioid receptor-like (ORL1) receptor

Mollereau, Catherine; Moulédous, Lionel

doi:10.1016/s0196-9781(00)00227-8

Cited by 219 publications

(152 citation statements)

References 87 publications

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“…The widespread distribution of benzodiazepine receptors likely accounts for the wide range of side effects associated with these agents (16). The NOP receptor has also been reported to be widely distributed throughout the CNS, and it is particularly prominent in the limbic system, including the amygdala, the septohippocampal region, periaqueductal gray matter, the locus coeruleus, and the dorsal raphe nucleus (17,18). This distribution suggests that targeting the NOP receptor may result in a number of adverse central effects.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Characterization of the Newly Synthesized Nociceptin/Orphanin FQ–Receptor Agonist 1-[1-(1-Methylcyclooctyl)-4-piperidinyl]-2-[(3R)-3-piperidinyl]-1H-benzimidazole as an Anxiolytic Agent

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Pharmacological Characterization of the Newly Synthesized Nociceptin/Orphanin FQ–Receptor Agonist 1-[1-(1-Methylcyclooctyl)-4-piperidinyl]-2-[(3R)-3-piperidinyl]-1H-benzimidazole as an Anxiolytic Agent

et al. 2008

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“…Neuroanatomical and immunohistochemical studies (Darland et al 1998;Mollereau and Mouledous 2000) have shown a wide distribution of N/OFQ and its receptor in various corticomesolimbic structures, including the amygdala, the bed nucleus of the stria terminalis, the nucleus accumbens (Nacc) and various fronto-cortical areas involved in the regulation of the motivational effect of drugs of abuse (Koob et al 1998;Wise 1998;Everitt and Wolf 2002).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of ethanol self-administration and of conditioned reinstatement of alcohol-seeking behaviour by the antiopioid peptide nociceptin/orphanin FQ in alcohol-preferring rats

et al. 2004

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Rationale-Nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the opioid-like orphan receptor NOP, was shown to reduce home-cage ethanol consumption, ethanol-induced conditioned place preference and stress-induced reinstatement of alcohol-seeking behaviour.Objectives-The present study, using genetically selected Marchigian Sardinian alcoholpreferring (msP) rats, was designed to evaluate the effect of this opioid peptide on 10% ethanol and 10% sucrose self-administration, under a fixed-ratio 1 (FR 1) or a progressive-ratio (PR) schedule of reinforcement. Furthermore, using an experimental model of relapse in which rats were trained to lever press for ethanol in the presence of the discriminative stimulus of an orange odour (S + ) and a 1-s cue light (CS + ) or for water in the presence of anise odour (S − ) and 1-s white noise (CS − ), the effect of N/oFQ on cue-induced reinstatement of extinguished ethanol responding was investigated.Correspondence to: Roberto Ciccocioppo, roberto.ciccocioppo@unicam.it. NIH Public AccessAuthor Manuscript Psychopharmacology (Berl). Author manuscript; available in PMC 2011 February 9. Conclusions-The present study demonstrates that the reinforcing effects of ethanol are markedly blunted by activation of the opioidergic N/OFQ receptor system. Moreover, the data provide evidence of the efficacy of N/OFQ to prevent reinstatement of ethanol-seeking behaviour elicited by environmental conditioned stimuli.

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“…bradycardia; depressor responses; opioid peptides THE PRESENCE OF A NOVEL G-protein-coupled receptor [opioid receptor-like receptor (ORL1) or OP 4 receptor] throughout the central nervous system has been repeatedly demonstrated (1, 3, 6, 12, 18, 20 -22). There is a high sequence similarity of this receptor with other opioid receptors (e.g., -, ␦-, and -receptors) (3,6,21,36). Nociceptin (orphanin FQ) (4, 25, 26), a heptadecapeptide, has been demonstrated to be an endogenous ligand of ORL1 receptor because of its high and selective affinity for this receptor and a very poor affinity for -, ␦-, and -opioid receptors.…”

mentioning

confidence: 99%

Mechanism of cardiovascular effects of nociceptin microinjected into the nucleus tractus solitarius of the rat

Chitravanshi

Sapru

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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.62, and 1.25 mmol/l of nociceptin into the medial nucleus tractus solitarius (mNTS) elicited decreases in mean arterial pressure (11 Ϯ 1.8, 20 Ϯ 2.1, 21.5 Ϯ 3.1, and 15.5 Ϯ 1.9 mmHg, respectively) and heart rate (14 Ϯ 2.7, 29 Ϯ 5.5, 39 Ϯ 5.2, and 17.5 Ϯ 3.1 beats/min, respectively). Because maximal responses were elicited by microinjections of 0.62 mmol/l nociceptin, this concentration was used for other experiments. Repeated microinjections of nociceptin (0.62 mmol/l) into the mNTS, at 20-min intervals, did not elicit tachyphylaxis. Bradycardia induced by microinjections of nociceptin into the mNTS was abolished by bilateral vagotomy. The decreases in mean arterial pressure and heart rate elicited by nociceptin into the mNTS were blocked by prior microinjections of the specific ORL1-receptor antagonist [N-Phe 1 ]-nociceptin-(1-13)-NH2 (9 mmol/l). Microinjections of the ORL1-receptor antagonist alone did not elicit a response. Prior combined microinjections of GABA A and GABAB receptor antagonists (2 mmol/l gabazine and 100 mmol/l 2-hydroxysaclofen, respectively) into the mNTS blocked the responses to microinjections of nociceptin at the same site. Prior microinjections of ionotropic glutamate receptor antagonists (2 mmol/l NBQX and 5 mmol/l D-AP7) also blocked responses to nociceptin microinjections into the mNTS. These results were confirmed by direct neuronal recordings. It was concluded that 1) nociceptin inhibits GABAergic neurons in the mNTS, 2) GABAergic neurons may normally inhibit the release of glutamate from the terminals of peripheral afferents in the mNTS, and 3) inhibition of GABAergic neurons by nociceptin results in an increase in the release of glutamate in the mNTS, which in turn elicits depressor and bradycardic responses via activation of ionotropic glutamate receptors on secondary mNTS neurons. bradycardia; depressor responses; opioid peptides THE PRESENCE OF A NOVEL G-protein-coupled receptor [opioid receptor-like receptor (ORL1) or OP 4 receptor] throughout the central nervous system has been repeatedly demonstrated (1, 3, 6, 12, 18, 20 -22). There is a high sequence similarity of this receptor with other opioid receptors (e.g., -, ␦-, and -receptors) (3,6,21,36). Nociceptin (orphanin FQ) (4, 25, 26), a heptadecapeptide, has been demonstrated to be an endogenous ligand of ORL1 receptor because of its high and selective affinity for this receptor and a very poor affinity for -, ␦-, and -opioid receptors. One notable difference between other opioid receptor agonists (e.g., endomorphins, enkephalins, and dynorphin A) and nociceptin is that naloxone blocks the effects of these opioid receptor agonists but not those of nociceptin (4,5,13,16,29).The presence of an endogenous ligand for ORL1 receptors (nociceptin or orphanin FQ) has been demonstrated throughout the central nervous system, including the nucleus tractus solitarius (NTS) (10, 23, 35). There are very few reports in which the cardiovascular effects of ORL1 receptor activation by nociceptin in the medial nucleus tractus solitarius (m...

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Tissue distribution of the opioid receptor-like (ORL1) receptor

Cited by 219 publications

References 87 publications

Pharmacological Characterization of the Newly Synthesized Nociceptin/Orphanin FQ–Receptor Agonist 1-[1-(1-Methylcyclooctyl)-4-piperidinyl]-2-[(3R)-3-piperidinyl]-1H-benzimidazole as an Anxiolytic Agent

Pharmacological Characterization of the Newly Synthesized Nociceptin/Orphanin FQ–Receptor Agonist 1-[1-(1-Methylcyclooctyl)-4-piperidinyl]-2-[(3R)-3-piperidinyl]-1H-benzimidazole as an Anxiolytic Agent

Attenuation of ethanol self-administration and of conditioned reinstatement of alcohol-seeking behaviour by the antiopioid peptide nociceptin/orphanin FQ in alcohol-preferring rats

Mechanism of cardiovascular effects of nociceptin microinjected into the nucleus tractus solitarius of the rat

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