γ-Aminobutyric acid in the lateral septal area is involved in mediation of the inhibition of hypothalamic angiotensin II-sensitive neurons induced by blood pressure increases in rats

Abstract

Previously, we have demonstrated that intravenous phenylephrine-induced increases in blood pressure inhibit angiotensin II-sensitive neurons via γ-aminobutyric acid (GABA) inputs in the anterior hypothalamic area (AHA). The lateral septal area (LSV) is also demonstrated to be involved in mediation of the baroreceptor reflex. To investigate central mechanisms involved in mediating the baroreceptor reflex, we examined whether GABA in the LSV is involved in mediation of the phenylephrine-induced inhibition of AHA angiotensin II-sensitive neurons. Microinjection of GABA into the LSV inhibited angiotensin II-sensitive neurons in the AHA of rats. The LSV GABA-induced inhibition of AHA neurons was abolished by pressure application of bicuculline onto the same AHA neurons. Intravenous injection of phenylephrine also inhibited AHA angiotensin II-sensitive neurons and the phenylephrine-induced inhibition of AHA neurons was abolished by microinjection of the GABAA receptor antagonist bicuculline into the LSV. In contrast, the LSV microinjection of bicuculline did not affect the inhibition of firing of AHA neurons induced by GABA pressure-applied in the AHA. These findings suggest that intravenous phenylephrine inhibits AHA angiotensin II-sensitive neurons via release of GABA in the LSV.