“…To determine the mechanisms involved in the mediation of Oct-induced drinking, water consumption was measured after intracerebroventricular injection of 0.1 g of Oct in rats pretreated as follows: 30 g of Cap (Sigma-Aldrich, Budapest) in 2 l or 10 g of Atr (atropine sulfate, Egis, Budapest) in 10 l were intracerebroventricularly injected 15 min before Oct, 10 g of Sar (Peninsula Laboratories, Belmont, CA) in 2 l were intracerebroventricularly administered 10 min before Oct, 100 g of Los (Merck Research Laboratories, Rahway, NJ) in 2 l were intracerebroventricularly injected 5 min before Oct, and 1 mg/kg of Nal (Narcanti, Du Pont Pharma, Bad Homburg, Germany) in a volume of 0.25 ml/100 g was subcutaneously injected 20 min before Oct. The doses of the antagonists corresponded to previously reported doses that were effective in inhibiting carbachol-or ANG II-induced drinking (15,21,30). This injection protocol required baseline measurements of water intake after double intracerebroventricular injections of PS/Veh (or subcutaneous ϩ intracerebroventricular PS for the experiments with Nal), after PS/Veh ϩ 0.1 g Oct, and after pretreatments with each of the compounds above ϩ intracerebroventricular injection of PS/Veh.…”