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.
D000315:Adrenalectomy; D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D001066:Appetite / Q000502:physiology*; D004327:Drinking Behavior / Q000502:physiology; D006624:Hippocampus / Q000502:physiology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D018161:Receptors, Mineralocorticoid; D012965:Sodium Chloride
D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D012965:Sodium Chloride; D000450:Aldosterone