The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats.

The central nucleus of the amygdala (CeA) is a critical region in regulating sodium intake, and interestingly, purinergic receptors reportedly related to fluid balance, are also expressed in CeA. In this study, we investigated whether the purinergic mechanisms of CeA were involved in regulating sodium intake. Male Sprague-Dawley rats had cannulas implanted bilaterally into the CeA and were sodium depleted with furosemide (FURO 20 mg/kg) plus 24 h-sodium deficient food fed. Bilateral injections of the P2X purinergic agonist, α,ß-methyleneadenosine 5'-triphosphate (α,ß-methylene ATP 1.0, 2.0, 4.0 nmol, respectively) into the CeA region induced dose-related reductions in sodium intake without affecting water intake. Injection of P2X purinergic antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS 4.0 nmol/0.5 µl) into the CeA region did not alter sodium and water intake, however, prior injection of PPADS into the CeA area abolished the inhibitory effects on sodium intake by α,ß-methylene ATP. Interestingly, prior injection of γ-aminobutyric acid type A (GABAA) receptor antagonist, bicuculline (4.0 nmol/0.5 µl) into the CeA region partially reversed the deficit of sodium intake induced by α,ß-methylene ATP. These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABAA receptor.

Natriorexigenic effect of DAMGO is decreased by blocking AT1 receptors in the central nucleus of the amygdala.

µ-Opioid receptor (µ-OR) activation with agonist [D-Ala², N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) in the central nucleus of the amygdala (CeA) induces sodium (0.3M NaCl) intake in rats. The purpose of this study was to examine the effects of pre-injections of losartan (AT1 angiotensin receptor antagonist) into the CeA on 0.3 M NaCl and water intake induced by DAMGO injected bilaterally in the same area in rats submitted to water deprivation-partial rehydration (WD-PR) and in rats treated with the diuretic furosemide (FURO) combined with a low dose of the angiotensin-converting enzyme inhibitor captopril (CAP) injected subcutaneously (FURO/CAP). Male Sprague-Dawley rats with stainless steel cannulas implanted bilaterally into the CeA were used. In WD-PR rats, bilateral injections of DAMGO (2 nmol in 0.5 µL) into the CeA induced 0.3 M NaCl and water intake, and pre-treatment with losartan (108 nmol in 0.5 µL) injected into the CeA reduced 0.3 M NaCl and water intake induced by DAMGO. In FURO/CAP rats, pre-treatment with losartan (108 nmol in 0.5 µL) injected into the CeA attenuated the increase in 0.3M NaCl and water intake induced by DAMGO (2 nmol in 0.5 µL) injected into the same site. The results suggest that the natriorexigenic effect of DAMGO injected into the CeA is facilitated by endogenous angiotensin II acting on AT1 receptors in the CeA, which drives rats to ingest large amounts of hypertonic NaCl.