5-HT2A and 5-HT2C/5-HT1B receptors are differentially involved in alcohol preference and consummatory behavior in cAA rats

Citation
S. Maurel et al., 5-HT2A and 5-HT2C/5-HT1B receptors are differentially involved in alcohol preference and consummatory behavior in cAA rats, PHARM BIO B, 62(1), 1999, pp. 89-96
Citations number
48
Categorie Soggetti
Neurosciences & Behavoir
Journal title
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
ISSN journal
00913057 → ACNP
Volume
62
Issue
1
Year of publication
1999
Pages
89 - 96
Database
ISI
SICI code
0091-3057(199901)62:1<89:5A5RAD>2.0.ZU;2-Z
Abstract
The present study aimed to investigate the role of serotonin 5-HT2A and 5-H T2C receptors in the control of alcohol preference and consummatory behavio r in alcohol-preferring cAA rats. Effects of the 5-HT2A/2C receptor agonist , DOI, the 5-HT2C/1B receptor agonist, mCPP, the 5-HT2A/2C receptor antagon ist, ritanserin, and the 5-HT2A receptor antagonist, MDL 100,907, on ethano l (EtOH, 10% v/v) preference and intake, as well as total fluid and food in take were evaluated in a 12-h limited-access two-bottle paradigm. DOI (0.3- 3 mg/kg, IF) reduced EtOH intake and preference, but not total fluid or foo d intake; whereas mCPP (1-10 mg/kg, SC) reduced EtOH, total fluid, and food intake. Therefore, it is concluded that DOI induces a specific and selecti ve antialcohol effect, whereas mCPP rather induces a general suppressive ef fect on consummatory behavior. Ritanserin (1-10 mg/kg, IF) did not affect E tOH intake and preference, nor total fluid and food consumption. MDL 100,90 7 (0.1-1 mg/kg, IF) induced only a small reduction of food intake at the hi ghest dose tested. Pretreatment with ritanserin (3 mg/kg, IF) and MDL 100,9 07 (0.3 mg/kg, IF) blocked the effects of DOI (3 mg/kg, IF), but not those of mCPP (10 mg/kg, IF). It is suggested that activation of 5-HT2C and/or 5- HT1B receptors results in a general decrease of consummatory behavior, wher eas activation of 5-HT2A receptors selectively decreases EtOH intake and pr eference, as assessed in the cAA rat model of alcoholism. (C) 1998 Elsevier Science Inc.