Suppression of GABAB receptor function in rat neocortical slices by amiloride.

Interactions of amiloride with GABAB receptors have been examined using spontaneously discharging rat neocortical slices. These discharges were suppressed by the GABAB receptor agonist baclofen (10 microM), and were prevented by amiloride and its analogs 5-(N,N-dimethyl)-amiloride, 5-(N-methyl-N-isobutyl)-amiloride and benzamil, but not by triamterene (100-500 microM). Each of these also increased the spontaneous discharge rate and reduced the discharge amplitude. The action of amiloride and its analogs in preventing the action of baclofen, may involve allosteric modification of the receptor binding sites via guanine nucleotide-binding proteins, or an indirect effect through antagonism of co-activated adenosine A1 receptors.