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| Research article summary (published 30 Aug 1997): |
Involvement of 5-hydroxytryptamine 2A (5-HT2A) receptors in the mediation of the discriminative stimulus properties of (+/-)DOI in rats.
Full Abstract
Rats were trained to discriminate between the 5-HT2A/2C receptor agonist (+/-)1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(+/-)DOI, 0.35 mg/kg] and saline using a two-lever drug discrimination procedure; afterwards, the effects of different 5-HT agonists and antagonists on the discriminative stimulus properties induced by (+/-)DOI were studied. In substitution tests, D-lysergic acid diethylamide (LSD, 0.02 and 0.04 mg/kg) and quipazine (0.5, 1.5 and 3 mg/kg), 5-HT2A/2C agonists, evoked dose-related responses to the (+/-)DOI-appropriate lever, while the non-selective 5-HT agonist 1-(3-chlorophenyl)piperazine (m-CPP, 0.1, 0.5 and 1 mg/kg), which has the highest binding affinity for 5-HT2C receptors, failed to show substitution. In antagonist studies, the discriminative stimulus effect of (+/-)DOI was completely antagonized by ketanserin (0.5 mg/kg) and cyproheptadine (0.5 mg/kg), preferential 5-HT2A receptor antagonists, and partially by the 5-HT2A/2C receptor antagonist mesulergine (0.25, 0.5 and 1.0 mg/kg) and the 5-HT2A/D2 antagonist spiperone (0.025, 0.05 and 0.1 mg/kg). The above data suggest that the discriminative stimulus effects of (+/-)DOI are predominantly mediated by 5-HT2A receptors.
Author information
Author/s: Chojnacka-Wójcik, E (E); Klodzinska, A (A);
Affiliation: Department of New Drug Research, Polish Academy of Sciences, Kraków, Poland.
Journal and publication information
Publication Type: Journal Article
Journal: Polish journal of pharmacology (Pol J Pharmacol), published in POLAND. (Language: eng)
Reference: -1997 Sep-Oct; vol 49 (issue 5) : pp 299-304
Dates: Created 1998/05/27; Completed 1998/05/27; Revised 2003/11/14;
PMID: 9566028, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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