Dipsogenic potentiation by sodium chloride but not by sucrose or polyethylene glycol in tuberomammillary-mediated polydipsia.

The aim of this study was to examine the dipsogenic mechanisms involved in the recently discovered tuberomammillary (TM)-mediated polydipsia. Rats with bilateral electrolytic lesions of each TM subnucleus underwent several dipsogenic treatments, both osmotic and volemic. Animals with ventral (E2) or medial TM lesions (E3 or E4) showed a potentiated hyperdipsic response to hypertonic sodium chloride administration but not to sucrose or polyethylene glycol treatments. The increase in response to sodium chloride was significantly greater in groups E3/E4 and E2 than in the non-lesioned group and in animals with polydipsia induced by lesion of the median eminence. As previously reported, hyperphagia was induced by lesion to ventral TM nuclei (E1 or E2), confirming a possible role for the TM complex in food intake. However, lesions in medial nuclei (E3 or E4) did not produce this increase in food intake. These results are interpreted in relation to the hypothalamic systems involved in food and water intake.