Clonidine suppression and its adrenoreceptor mediation in schedule-induced polydipsia

Rats were trained in a fixed-interval, one-minute (FI 1 min) food reinforcement schedule for 1 hour daily at reduced body weight until their lever presses, licks and water intake all became stabilized for 6 days. Two experiments were performed to examine the function of sympathetic activity in schedule-induced polydipsia. In experiment 1, intracerebroventricular injection of clonidine (0.75-37.5 nmol) produced a dose-related suppression of schedule-induced drinking and licking and schedule-dependent lever pressing; these effects were later attenuated by yohimbine (5 nmol) pretreatment. Prazosin (10 nmol) also decreased clonidine-induced suppression of lever pressing, whereas neither prazosin (10 nmol) nor naloxone (10 nmol) caused any alteration in the suppression effects of clonidine on drinking and licking. None of these antagonists alone changed an individual rat's preestablished behavioral baselines. In experiment 2, the endogenous catecholamine levels, were determined in frontal cortex, hypothalamus, brainstem, dorsal obex area and adrenal glands. During the SIP situation, both the epinephrine level in adrenal glands and the norepinephrine level in hypothalamus were elevated.