Sodium and water intake are not affected by GABAC receptor activation in the lateral parabrachial nucleus of sodium-depleted rats

The activation of GABAergic receptors, GABA_A and GABA_B, in the lateral parabrachial nucleus (LPBN) increases water and sodium intake in satiated and fluid-depleted rats. The present study investigated the presence of the GABA_C receptor in the LPBN, its involvement in water and sodium intake, and its effects on cardiovascular parameters during the acute fluid depletion induced by furosemide combined with captopril (Furo/Cap). One group of male Wistar rats (290–300 g) with bilateral stainless steel LPBN cannulas was used to test the effects of a GABA_C receptor agonist and antagonist on the fluid intake and cardiovascular parameters. We investigated the effects of bilateral LPBN injections of trans-4-aminocrotonic acid (TACA) on the intake of water and 0.3 M NaCl induced by acute fluid depletion (subcutaneous injection of Furo/Cap). c-Fos expression increased (P<0.05), suggesting LPBN neuronal activation. The injection of different doses of TACA (0.5, 2.0 and 160 nmol) in the LPBN did not change the sodium or water intake in Furo/Cap-treated rats (P > 0.05). Treatment with the GABA_C receptor antagonist (Z)-3-(aminoiminomethyl)thio]prop-2-enoic acid sulfate (ZAPA, 10 nmol) or with ZAPA (10 nmol) plus TACA (160 nmol) did not change the sodium or water intake compared with that for vehicle (saline) (P > 0.05). Bilateral injections of the GABA_C agonist in the LPBN of Furo/Cap-treated rats did not affect the mean arterial pressure (MAP) or heart rate (HR). The GABA_C receptor expression in the LPBN was confirmed by the presence of a 50 kDa band. Although LPBN neurons might express GABA_C receptors, their activation produced no change in water and sodium intake or in the cardiovascular parameters in the acute fluid depletion rats. Therefore, the GABA_C receptors in the LPBN might not interfere with fluid and blood pressure regulation.