FOS EXPRESSION IN RAT-BRAIN DURING DEPLETION-INDUCED THIRST AND SALT APPETITE

The expression of Fos protein (Fos immunoreactivity, Fos-ir) was mappe d in the brain of rats subjected to an angiotensin-dependent model of thirst and salt appetite. The physiological state associated with wate r and sodium ingestion was produced by the concurrent subcutaneous adm inistration of the diuretic furosemide (10 mg/kg) and a low dose of th e angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Fu ro/Cap treatment). The animals were killed 2 h posttreatment, and the brains were processed for Fos-ir to assess neural activation. Furo/Cap treatment significantly increased Fos-ir density above baseline level s both in structures of the lamina terminalis and hypothalamus known t o mediate the actions of ANG II and in hindbrain regions associated wi th blood volume and pressure regulation. Furo/Cap treatment also typic ally increased Fos-ir density in these structures above levels observe d after administration of furosemide or captopril separately. Fos-ir w as reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain. The present work provides further evidence that areas of lamina terminalis subserve angiotensin-dependent thirst and salt appe tite.