PMID- 26735639 OWN - NLM STAT- PubMed-not-MEDLINE DCOM- 20160108 LR - 20160107 IS - 1355-6215 (Print) IS - 1355-6215 (Linking) VI - 2 IP - 2 DP - 1997 Apr TI - Involvement of CNS cholinergic systems in alcohol drinking of P rats. PG - 215-23 LID - 10.1080/13556219772769 [doi] AB - Experiments were undertaken to determine if CNS muscarinic- and nicotinic-cholinergic receptors are involved in regulating alcohol drinking of rats from the selectively-bred alcohol-preferring P line. Intracerebroventricular (i.c.v.) drug infusions were administered into the lateral ventricle of female P rats 15 minutes before ethanol access. The muscarinic antagonists pirenzepine and scopolamine were tested on limited access (4 hours/day) to a 10% (v/v) ethanol solution. Food and water were available ad libitum. Nicotine and the nicotinic antagonist mecamylamine were tested on limited access (4 hours/day) to 10% (v/v) ethanol and 0.0125% saccharin solutions. Food was available ad libitum and water was available during the remaining 20 hours. The baseline ethanol intakes ranged between an average of 3.0 +/- 0.3 g/kg/4 hours and 3.4 +/- 0.3 g/kg/4 hours. Administration of 40-100 m g pirenzepine (M1-selective antagonist) had no effect on ethanol, food or water consumption. However, 20-80 m g scopolamine, a non-selective muscarinic antagonist, dosedependently decreased ethanol intake as much as 60% (p < 0.05) without altering food or water consumption. The nicotinic antagonist mecamylamine (20-120 m g) did not alter ethanol intake, but nicotine (40-80 m g) dose-dependently decreased ethanol drinking as much as 60% within the first 30 minutes (p < 0.05) without an effect on saccharin intake. The results suggest that: (a), muscarinic receptors, with the possible exception of the M1 subtype, are involved in regulating alcohol drinking and (b), activation of nicotinic receptors can reduce alcohol drinking of the P line of rats. FAU - Katner, S N AU - Katner SN AD - Program in Medical Neurobiology, Institute of Psychiatric Research, Departments of Psychiatry, Medicine and Biochemistry, Indiana University School of Medicine and VA Medical Center & Department of Psychology, Purdue School of Science, Indiana University-Purdue University, Indianapolis, USA. FAU - McBRIDE, W J AU - McBRIDE WJ AD - Program in Medical Neurobiology, Institute of Psychiatric Research, Departments of Psychiatry, Medicine and Biochemistry, Indiana University School of Medicine and VA Medical Center & Department of Psychology, Purdue School of Science, Indiana University-Purdue University, Indianapolis, USA. FAU - Lumeng, L AU - Lumeng L AD - Program in Medical Neurobiology, Institute of Psychiatric Research, Departments of Psychiatry, Medicine and Biochemistry, Indiana University School of Medicine and VA Medical Center & Department of Psychology, Purdue School of Science, Indiana University-Purdue University, Indianapolis, USA. FAU - Li, T K AU - Li TK AD - Program in Medical Neurobiology, Institute of Psychiatric Research, Departments of Psychiatry, Medicine and Biochemistry, Indiana University School of Medicine and VA Medical Center & Department of Psychology, Purdue School of Science, Indiana University-Purdue University, Indianapolis, USA. FAU - Murphy, J M AU - Murphy JM AD - Program in Medical Neurobiology, Institute of Psychiatric Research, Departments of Psychiatry, Medicine and Biochemistry, Indiana University School of Medicine and VA Medical Center & Department of Psychology, Purdue School of Science, Indiana University-Purdue University, Indianapolis, USA. LA - eng PT - Journal Article PL - United States TA - Addict Biol JT - Addiction biology JID - 9604935 EDAT- 1997/04/01 00:00 MHDA- 1997/04/01 00:01 CRDT- 2016/01/07 06:00 PHST- 2016/01/07 06:00 [entrez] PHST- 1997/04/01 00:00 [pubmed] PHST- 1997/04/01 00:01 [medline] AID - 10.1080/13556219772769 [doi] PST - ppublish SO - Addict Biol. 1997 Apr;2(2):215-23. doi: 10.1080/13556219772769.