Changes in α-adrenoceptor number and function in brains of morphine-dependent rats
References (32)
- et al.
Morphine tolerance and dependence in the locus coeruleus: single cell studies in brain slices
European J. Pharmacol.
(1983) - et al.
Characterization of alpha1- and alpha2-adrenoceptors
Int. Rev. Neurobiol.
(1983) - et al.
Naltrexone precipitated opiate withdrawal in methadone addicted human subjects: evidence for noradrenergic hyperactivity
Life Sci.
(1984) - et al.
Platelet α2-adrenoceptors in heroin addicts during withdrawal and after treatment with clonidine
European J. Pharmacol.
(1985) - et al.
Protein measurement with the Folin phenol reagent
J. Biol. Chem.
(1951) A practical computer-based approach to the analysis of radioligand binding experiments
Comput. Prog. Biomed.
(1983)- et al.
Changes in central adrenoceptor function after long-term opiate treatment
Neuropeptides
(1984) - et al.
Changes in cortical beta adrenergic receptor density and neuronal sensitivy to norepinephrine accompany morphine dependence and withdrawal
Brain Res.
(1987) - et al.
LIGAND: a versatile computerized approach for characterization of ligand-binding systems
Anal. Biochem.
(1980) - et al.
Alpha2-adrenorectors in rat brain are decreased after long-term tricyclic antidepressant drug treatment
Brain Res.
(1981)
Changes in alpha2 adrenoreceptors in various areas of the rat brain after long-term administration of ‘mu’ and ‘kappa’ opiate agonist
Life Sci.
Chronic opiate treatment does not modify α2-adrenergic receptors in rat cerebral cortex, kidney and in the neurotumor cell line NCB20
European J. Pharmacol.
Tolerance of locus coeruleus neurons to morphine and suppression of withdrawal response by clonidine
Nature
Cellular mechanisms of opioid tolerance: studies in single brain neurons
Mol. Pharmacol.
Catecholamine biosynthesis in brains of rats treated with morphine
Science
α2-Adrenoceptor-mediatedinhibition of platelet adenylate cyclase activity in heroin addicts in abstinence
Psychopharmacology
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Molecular Changes in Opioid Addiction: The Role of Adenylyl Cyclase and cAMP/PKA System
2016, Progress in Molecular Biology and Translational ScienceCitation Excerpt :In contrast, no change in α2-adrenoreceptor density was observed in a neurotumor cell line 89 while another study showed an increase in density.90 In hippocampal slices, chronic administration of morphine reduced α2-adrenoreceptor binding.88 Clonidine has been used successfully in the treatment of acute opiate withdrawal.91
Yokukansan inhibits morphine tolerance and physical dependence in mice: The role of α<inf>2A</inf>-adrenoceptor
2012, NeuroscienceCitation Excerpt :Therefore, provision of α2-AR antagonists during morphine exposure might be expected to counteract morphine-induced neuronal hypoactivity, thus preventing the subsequent hyperactivity of LC noradrenergic neurons during morphine withdrawal. However, an early study reported that morphine dependence and withdrawal led to decreases in the expression of α2-AR in many brain regions, as well as increases in noradrenaline release from hippocampal slices in response to field stimulation (Smith et al., 1989). Furthermore, Alonso et al. (2007) reported that chronic morphine treatment decreased the mRNA expression levels of α2A- and α2C-ARs in the hippocampus, whereas pretreatment with yohimbine blocked this decrease.
The contribution of α<inf>2</inf>-adrenoceptor and opioid receptor mechanisms to antinociception differs in Lewis and Fischer 344 rats
2003, European Journal of PharmacologyGenetic variability in morphine sensitivity and tolerance between different strains of rats
2000, Brain ResearchCitation Excerpt :On the other hand, involvement of the opioid system in morphine sensitivity of the SD-U rats was demonstrated as morphine antinociception was reversed by naloxone. This ruled out the possibility that the observed differences may be due to the participation of other neurotransmission systems that have been previously implicated in morphine antinociception [15,22]. Tolerance can be described as the adaptation of a biological system to a continued or repeated effect of a drug, and as such, be defined as a loss of drug potency after repeated administration.