Abstract
Although the anteroventral third ventricular region (AV3V), a pivotal forebrain area for autonomic functions, contains the receptors (-R) for GABA that might operate in association with those for excitatory amino acids, their roles in regulating ADH release and related phenomena have not been examined as yet. This study aimed to pursue the issue through experiments in conscious rats with indwelling cerebral and vascular cannulae. Infusion sites of drugs in the brain were identified through histological inspections. Administrations of a GABA(A) receptor antagonist bicuculline (BCC) into the AV3V caused prompt and remarkable augmentations in plasma ADH, osmolality, glucose, arterial pressure and heart rate, without affecting plasma electrolytes. When BCC was injected into the cerebral ventricle, relatively smaller or no responses were provoked in the variables. In contrast, AV3V injections of a GABA(B)-R antagonist phaclofen did not show any effects on those variables. The responses to AV3V applications of BCC were inhibited by preadministrations of a GABA(A)-R agonist muscimol, the treatments that affected none of the variables when injected alone. The applications of Glu-R antagonists MK-801 or NBQX were also potent to abolish the responses to AV3V BCC. These results suggest that in the AV3V GABA neurons may tonically operate to prevent ADH secretion and cardiovascular functions via the mechanisms related to glutamatergic neuronal activity. [J Physiol Sci. 2007;57 Suppl:S75]
