RT Journal Article SR Electronic T1 Solubilization of a [3H]Cimetidine Binding Site from Rat Brain JF Molecular Pharmacology JO Mol Pharmacol FD American Society for Pharmacology and Experimental Therapeutics SP 240 OP 243 VO 20 IS 2 A1 N. SUBRAMANIAN A1 T. A. SLOTKIN YR 1981 UL http://molpharm.aspetjournals.org/content/20/2/240.abstract AB A binding site for [3H]cimetidine was obtained from rat brain membranes solubilized with digitonin. The site displayed saturability, high affinity, and drug specificity for imidazole H-2 antagonists and was able to bind ligand at physiological temperatures. The regional distribution of binding sites paralleled that of neuronal histamine projections. Displacement of binding did not occur readily with H-2 agonists, and, although 2-guanidino-4-[2-(2-cyano-3-methyl-guanidino)ethyl-thiomethyl]thiazole (ICI 125,211, (a non-imidazole H-2 antagonist) displaced [3H]cimetidine, it was less potent than imidazole antagonists. Micromolar concentrations of clonidine, a substance thought to stimulate a central imidazole H-2 receptor subtype, were able to displace [3H]cimetidine binding, and chronic treatment of rats with clonidine in vivo resulted in down-regulation of the sites. These data suggest that the solubilized [3H]cimetidine binding site is associated with the putative clonidine-sensitive H-2 receptor subtype.