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pubmed-article:2576452pubmed:abstractTextThis study examined the effect of chronic clomipramine administration on opioid mu- and kappa-binding sites. Clomipramine (5 mg kg-1 day-1) or saline was administered to rats via osmotic minipumps for 3 days or 28 days. Lysed-P2 brain membranes were prepared and preincubated for 60 min without (control membranes) or with 1 microM of the mu-selective acylating agent, 2-(4-ethoxybenzyl)-1-diethylaminoethyl-5-isothiocyanatobenzimid azole-HC1 (BIT), to deplete membranes of mu-binding sites. [3H]6-Desoxy-6 beta-fluoronaltrexone ( [3H]cyclo FOXY) was used to label mu and kappa-binding sites. Weighted nonlinear least squares analysis of cycloFOXY binding surfaces permitted determination of the Kd and Bmax values of mu- and kappa-binding sites in control and treated rats. Subacute (3 days) administration of rats with clomipramine had no significant effect on [3H]cycloFOXY binding. Chronic (28 days) administration of clomipramine produced a small (approximately 10%) but statistically significant decrease in the Bmax. These findings are discussed in reference to other studies that have examined the effect of chronic antidepressant administration on opioid receptors, and speculate that the endogenous opioid systems may play a role in obsessive-compulsive disorder.lld:pubmed
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pubmed-article:2576452pubmed:articleTitleApparent down-regulation of rat brain mu- and kappa-opioid binding sites labelled with [3H]cycloFOXY following chronic administration of the potent 5-hydroxytryptamine reuptake blocker, clomipramine.lld:pubmed
pubmed-article:2576452pubmed:affiliationSection on Clinical Neuropharmacology, National Institute of Mental Health, Bethesda, Maryland 20892.lld:pubmed
pubmed-article:2576452pubmed:publicationTypeJournal Articlelld:pubmed