INCREASED ACETYLCHOLINE AND QUISQUALATE RESPONSIVENESS AFTER BLOCKADE OF GABA (B)-RECEPTORS

Thc aim of this study was to gain further insight into the function of cortical GABA(B) receptors. In chloral hydrate-anaesthetized rats, microiontophoretic administration of the GABA(B) receptor blocker CGP 35348 induced a moderate increase in firing of spontaneously active neurons in the rostral and caudal sensorimotor cortex. This increase in cell firing was accompanied by a reduction in the baclofen-induced inhibition of cell activity. In contrast to the GABA(A) receptor antagonist bicuculline methiodide, CGP 35348 did not induce any paroxysmal discharges. Thc excitatory responses of rostral cortical neurons elicited by iontophoretically applied acetylcholine and quisqualate were potentiated in most neurons after both microiontophoretic and intravenous administration of CGP 35348. The potentiation was observed in the absence of any change in thc spontaneous firing rate. These effects were dose-dependent for both routes of administration. The potentiation of the quisqualate response was reversed by intravenously applied baclofen. In conclusion, these findings suggest that cortical GABA(B) receptors are involved in the control of cortical neuronal excitability.