POLYDIPSIA AND DOPAMINE - BEHAVIORAL-EFFECTS OF DOPAMINE D1 AND D2 RECEPTOR AGONISTS AND ANTAGONISTS

Substantial evidence implicates dopaminergic neural systems in the occ urrence of polydipsia in both animals and humans. Two experiments were conducted in order to specify the behavioral mechanisms whereby manip ulation of dopaminergic neural transmission can affect scheduled-induc ed polydipsia (SIP). The role of dopamine D1 and D2 receptors was inve stigated by comparing the behavioral effects of dopamine D1 agonists ( SKF 38393 and SKF 82958) and antagonists (SCH 23390 and SKF 83566) to those of a dopamine D2 agonist (quinpirole) and antagonist (haloperido l) by using an animal model of excessive water consumption, drinking e voked in the SIP paradigm. Additionally, the behavioral effects of the se relatively specific compounds were compared to those of the indirec t agonist d-amphetamine sulfate and the nondopaminergic drug, diazepam . All of the drugs produced dose-related decreases in SIP. With the ex ception of SKF 38393 and SCH 23390, the decreased drinking appeared to be a behaviorally nonspecific drug effect in that changes in activity consistently preceded or accompanied reductions in water consumption. Some of the drugs tested, including quinpirole, haloperidol and SKF 8 3566, also produced changes in behavior consistent with decreased hung er, which may have also contributed to the reductions in SIP. These re sults are generally suggestive that dopamine neural systems are involv ed mainly in the motor or performance aspects of established SIP and t hat disruptions in established SIP produced by dopamine agonists or an tagonists may result from a change in the balance of activation of dop amine D1 and D2 receptors. These results may be relevant to understand ing the factors influencing polydipsia in humans.