Rehydration process from salt-loading: recovery of vasopressin and its coexisting galanin, dynorphin and tyrosine hydroxylase immunoreactivities in the supraoptic and paraventricular nuclei.

Salt-loading induces profound metabolic changes in magnocellular vasopressin (AVP)-containing neurons, including changes in levels of coexisting peptides and tyrosine hydroxylase (TH). Although many studies have been conducted on salt-loading, little information is available on the recovery processes following its cessation. In the present study, we investigated the changes in AVP, galanin (Gal), dynorphin B (Dyn-B), and TH immunoreactivities in the rat supraoptic nucleus (SON) and paraventricular nucleus (PVN) by immunocytochemistry using specific antisera against these substances. Salt-loading was induced in rats by dissolving 2% NaCl in their drinking water for 7 days. These animals were then allowed free access to fresh water for 2, 4, or 7 days prior to sacrifice. In the SON at the 7th day of salt-loading, AVP, Gal and Dyn-B immunoreactivities decreased in contrast to the marked increase in TH-immunoreactivity compared to those of control rats with free access to water. After a recovery period with free access to water, AVP and Gal immunoreactivities increased with time and returned to the control level at the 7th day. However, Dyn-B immunoreactivity did not recover even at the 7th day. Dehydration-induced TH-immunoreactive neurons almost disappeared at the 7th day. Immunoreactivities for these substances in the PVN showed a similar time course as that in the SON. These findings suggest that AVP and substances coexisting with it change with different time courses in magnocellular neurons following cessation of salt-loading.