Experiments on the neuropsychology of thirst.

We report the results of a series of experiments whose main objectives are: (a) the identification of neural receptors for thirst; and (b) other neural structures of critical importance for thirst and drinking behavior. We have used results from hypertonic challenges during acute unit and multiple-unit recording experiments to identify responsive brain areas for behavioral study in chronic experiments. Results include the following. Single cells in the lateral preoptic area (LPOA) responded to injections of hypertonic saline into the carotid artery in a dose-related manner. Multiple unit activity (MUA) reactions were invariably facilitatory to challenge, and were much greater in the LPOA than in the medial preoptic area (MPOA). In unit and MUA recording we found extremely osmosensitive sites in the dorsal midbrain. Comparing the effects of NaCl vs sucrose as challenges via the intracarotid artery we found that LPOA MUA responses to sucrose were at least as strong and latencies as short as those to NaCl. These results support osmoreceptor theory, as revised by Epstein and his co-workers, and they are opposed to Andersson's sodium receptor theory. Hypertonic NaCl and sucrose solutions (but not artificial CSF controls) injected into the lateral ventricle were effective in producing strong MUA reactions, which typically were inhibition followed by facilitation. These and other findings support the following conclusions. (a) The LPOA appears to be a vital part of the neural mechanism for thirst and it is a probable site of osmoreceptors. (b) In addition, the LPOA seems to be a receiving area connected with putative periventricular neural receptors. (c) Intraventricular (i.v.t.) angiotensin II seems to be a much stronger dipsogen than hypertonic NaCl i.v.t., which in higher concentrations elicited stereotyped running.