NMDA lesions of lateral hypothalamus enhance the acquisition of schedule-induced polydipsia

Schedule-induced polydipsia (SIP) is affected by damage to various limbic structures that have connections with the lateral hypothalamus. The present experiment sought to determine whether or not SIP could be induced in rats bearing NMDA-induced lesions of the lateral hypothalamus. Following surgery, lesioned rats lost weight and were hypophagic and hypodipsic. Drinking, in response to systemic injection of hypertonic saline, was impaired in lesioned rats. Prior to testing for SIP, all rats were placed on a food-restriction regime to maintain body weight at 85% of normal. There was no statistically significant difference in mean body weight between lesioned and control groups before deprivation began, though lesioned rats were hypodipsic in their home cages. The lateral hypothalamic-lesioned rats acquired SIP significantly more rapidly than controls over the first six sessions, but over four following sessions no differences were present. The enhanced acquisition of SIP by lateral hypothalamic-lesioned rats cannot be accounted for by postoperative recovery of body weight or by hypodipsia in the home cage, neither of which correlated with SIP. It is suggested that the lateral hypothalamus has a role in cueing appropriate and inhibiting inappropriate behavior in conditions of motivational excitement. SIP is suggested to have two CNS components--one excitatory and one inhibitory.