Abstract
The forebrain osmosensitive area called the anteroventral third ventricular region (AV3V) possesses gamma-aminobutyric acid (GABA) receptors (-R) that might cooperate with glutamatergic (Glu)-R shown by us to be involved in the osmotic ADH secretion. However, roles of the GABA-R in regulating ADH and related factors in the absence or presence of hyperosmolality remain unknown. The present study aimed to explore this issue through experiments in awake rats implanted chronically with indwelling vascular and brain cannulae. Infusion sites in the brain were determined by histological inspections. AV3V application of bicuculline (Bic), a GABA(A)-R antagonist (Ant), but not phaclofen, a GABA(B)-R Ant, elicited marked rises in plasma ADH, osmolality (Osm), glucose, arterial pressure (AP) and heart rate, without causing significant changes in plasma electrolytes. These effects of Bic were prevented by preadministering a GABA(A)-R agonist muscimol (Mus), or a Glu-R Ant MK-801 or NBQX. When infused intravenously 2.5 M NaCl augmented plasma ADH, Osm, sodium and AP gradually with time. The responses of ADH and AP were abolished by AV3V application of Mus, whereas in the absence of the osmotic load the Mus treatment affected none of the variables monitored. From these results, we concluded that the osmotic load may inhibit AV3V GABAergic activity to promote ADH secretion through potentiation of local Glu activity. [J Physiol Sci. 2008;58 Suppl:S138]
