Mineralocorticoid regulation of salt intake is preserved in hippocampectomized rats.

Considering the high concentration of binding sites for [3H]-aldosterone in the hippocampus, a relationship between these sites and the regulation of sodium appetite by aldosterone was investigated. After surgical hippocampectomy, rats showed an approximately 80% depletion of [3H]-aldosterone binding sites. In spite of this reduction, hippocampectomized rats developed a sodium appetite after adrenalectomy; this sodium appetite was suppressed by continuous administration of aldosterone, a response similar to the pattern found in normal rats. These results suggest that the hippocampus is not the main target of the effect of the hormone on salt intake.