ArticleUpregulation of the opioid receptor complex by the chronic administration of morphine: A biochemical marker related to the development of tolerance and dependence
References (83)
- et al.
Effects of stress and beta-funaltrexamine pretreatment on morphine analgesia and opioid binding in rats
Life Sci.
(1987) - et al.
Role of serotonergic input in the down-regulation of beta-adrenoreceptors following long-term clorgyline treatment
Eur. J. Pharmacol.
(1988) - et al.
The effects of receptor selective opioid peptides on morphine-induced analgesia
Eur. J. Pharmacol.
(1982) - et al.
Chronic morphine increases μ-opiate receptor binding in rat brain: A quantitative autoradiographic study
Brain Res.
(1989) - et al.
Decrease of tolerance development to morphine by 5-hydroxytryptophan and some related drugs
Eur. J. Pharmacol.
(1973) - et al.
Chronic administration of morphine and naltrexone up-regulate 3H-[D-ala2,D-leu5]enkephalin binding sites by different mechanisms
Neuropharmacology
(1988) - et al.
Dynorphin: A possible modulatory peptide on morphine or beta-endorphin analgesia in mouse
Eur. J. Pharmacol.
(1981) - et al.
Existence of antiopiate systems as illustrated by MIF-1/Tyr-MIF-1
Life Sci.
(1986) - et al.
Differential activity of the endogenous antiopiate Tyr-MIF-1 after various intensities of stress
Neurosci. Lett.
(1988) - et al.
Influence of 5,6,-dihydroxytryptamine on morphine tolerance and physical dependence
Eur. J. Pharmacol.
(1973)
Repeated electroconvulsive shock or chronic morphine increases the number of 3H-D-ala2,D-leu5-enkephalin binding sites in rat brain
Life Sci.
Tyr-MIF-1 acts as an opiate antagonist in the tail-flick test
Pharmacol. Biochem. Behav.
IgG from antiserum against endogenous mammalian FRMF-NH2-related peptides augments morphine- and stress-induced analgesia in mice
Peptides
The role of central serotoninergic neurotransmission in the morphine abstinence syndrome in rats
Drug Alcohol Depend.
Opiate and peptide interaction: Effect of enkephalins on morphine analgesia
Eur. J. Pharmacol.
Inhibition of morphine tolerance and physical dependence development and brain serotonin synthesis by cyclohexamide
Biochem. Pharmacol.
FMRF-NH2-like mammalian octapeptide: Possible role in opiate dependence and abstinence
Peptides
Regulation of G proteins by chronic morphine in the rat locus coeruleus
Brain Res.
Morphine-induced opioid receptor down-regulation detected in intact adult rat brain cells
Eur. J. Pharmacol.
Multidimensional analysis of ligand binding data: Application to opioid receptors
Neuropeptides
Preparation of rat brain membranes greatly enriched with either type-I-delta or type-II-delta opiate binding sites using site directed alkylating agents
Neuropeptides
Chronic administration of morphine and naltrexone up-regulate opioid binding sites labeled by 3H[D-ala2-MePhe4,Gly-ol5]enkephalin: Evidence for two mu binding sites
Eur. J. Pharmacol.
Tritiated-6-beta-fluoro-6-desoxy-oxymorphone ([3H]FOXY): A new ligand and photoaffinity probe for the mu opioid receptors
Neuropeptides
Morphine tolerance increases mu-noncompetitive delta binding sites
Eur. J. Pharmacol.
Chronic morphine up-regulates a mu-opiate binding site labeled by 3H-cycloFOXY: A novel opiate antagonist suitable for positron emission tomography
Eur. J. Pharmacol.
Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture
Brain Res.
The irreversible narcotic antagonistic and reversible agonistic properties of the fumaramate methyl ester derivative of naltrexone
Eur. J. Pharmacol.
The anticonvulsant effects of DADL are primarily mediated by activation of delta opioid receptors: Interaction between delta and mu-receptor antagonists
Life Sci.
Mu and delta receptors: Their role in analgesia and in the differential effects of opioid peptides on analgesia
Life Sci.
Opioid receptor binding characteristics of the nonequilibrium mu antagonist, beta-funaltrexamine (beta-FNA)
Eur. J. Pharmacol.
Increased analgesic potency of morphine and increased brain opioid binding sites in the rat following chronic naltrexone treatment
Life Sci.
Chronic, but not acute, administration of morphine alters antiopiate (tyr-MIF-1) binding sites in rat brain
Life Sci.
Central serotonergic mechanisms and development of morphine dependence
Drug Alcohol Depend.
Pharmacological studies with an alkylating narcotic agonist, chloroxymorphamine, and antagonist, chlornaltrexamine
J. Pharmacol. Exp. Ther.
Opioid receptor reserve in normal and morphine-tolerant guinea pig ileum myenteric plexus
A general therory of the genesis of drug dependence by induction of receptors
Nature
Antagonism of morphine-induced analgesia, tolerance and dependence by alpha-melanocyte-stimulating hormone
J. Pharmacol. Exp. Ther.
Receptor adaptations to centrally administered drugs
Annu. Rev. Pharmacol. Toxicol.
Multiple opiate receptors in endotoxic shock: Evidence for delta involvement and mu-delta interactions in vivo
Implications of methadone maintenance for theories of narcotic addiction
JAMA
Comparison of thyrotropin-releasing hormone (TRH), naloxone, and dexamethasone treatments in experimental spinal injury
Neurology
Cited by (58)
‘Not at all what I had expected’: Discontinuing treatment with extended-release naltrexone (XR-NTX): A qualitative study
2022, Journal of Substance Abuse TreatmentCitation Excerpt :Studies have proposed that prolonged opioid use, and thus continued exposure to mu agonists, can result in kappa receptor system overdrive (Banks, 2020; Chavkin & Koob, 2016). This overdrive may lead to dysphoric mood states, which may be part of a prolonged abstinence reaction, symptoms which may be further increased by naltrexone mu opioid receptor blockade (Rothman, 1992; Rothman et al., 1991). Participants who tested the blockade with buprenorphine may have achieved an effect where buprenorphine reinforced NTX’ weak kappa and delta antagonism, producing an anti-depressant effect (Ehrich et al., 2015; Fava et al., 2020; Karp et al., 2014; McCann, 2008), which research has suggested affects dysphoric mood and opioid-seeking behavior associated with prolonged opioid withdrawal (Gerra et al., 2006; Rothman et al., 2000).
Attenuation of morphine-induced dependence and tolerance by ceftriaxone and amitriptyline in mice
2014, Acta Anaesthesiologica TaiwanicaCitation Excerpt :Between-system adaptations, such as the pain facilitatory systems (opiate-activated opponent systems), also play an important role in the development of opioid-induced tolerance and dependence.5–8 The activation of the ionotropic N-methyl-d-aspartate (NMDA) subtype of glutamate receptors has been implicated in the development of morphine analgesic tolerance and dependence.7,9–11 Chronic opioid treatment resulted in the activation of protein kinase C and translocation that phosphorylates the NMDA receptor-gated Ca channel, leading to potentiation of NMDA receptor activity.
Stabilization of the μ-opioid receptor by truncated single transmembrane splice variants through a chaperone-like action
2013, Journal of Biological ChemistryCitation Excerpt :Both agonists and antagonists can up-regulate opioid receptors at the protein level through promoting correct conformation or folding of the receptor proteins by escaping the ERAD pathway (60–64). Similar observations were made as early as 1973, when it was reported that administration of opiates in vivo increased opioid receptor binding in the brain by as much as 70% with a concomitant enhanced sensitivity toward opioids (65–69). Presumably, the single TM variants act through a physical association with the full-length variant, supported by our evidence that they can physically associate.
New horizons for therapeutics in drug and alcohol abuse
2010, Pharmacology and TherapeuticsChronic morphine treatment up-regulates mu opioid receptor binding in cells lacking filamin A
2007, Brain ResearchCitation Excerpt :The effects of chronic morphine administration on MOP-binding site density have also been investigated in animal brain and brain regions. These studies produced all possible changes in MOP density, namely, up-regulation (Besse et al., 1992; Brady et al., 1989; Fabian et al., 2002, 2003; Holaday et al., 1982; Ray et al., 2004; Rothman et al., 1991; Schmidt et al., 2003; Vigano et al., 2003), down-regulation (Bhargava and Gulati, 1990; Meuser et al., 2003; Werling et al., 1989) or no change (Polastron et al., 1994; Stafford et al., 2001; Turchan et al., 1999). Some of these results appear to be regional differences, but others, performed on whole brain or the same regions of the same animal, appear to be discrepancies between different laboratories.
Buprenorphine treatment outcome in dually diagnosed heroin dependent patients: A retrospective study
2006, Progress in Neuro-Psychopharmacology and Biological Psychiatry