GABAB receptors enhance excitatory responses in isolated rat retinal ganglion cells

GABA(B) receptors (GABA(B)Rs) suppress voltage-gated calcium channels and activate G-protein coupled potassium channels (GIRK and TREK channels), both mechanisms serving to inhibit neurons. In isolated rat retinal spiking neurons, GABA(B)Rs produce both actions but the net effect is to enhance excitatory signals. This is because GABA(B)Rs selectively suppress N-type calcium channels, which in turn are specifically linked to BK channels. Consequently, when GABA(B)Rs are stimulated there is a reduction in outward current, allowing neurons to extend their level of depolarization. Whereas many retinal neurons use L-type channels to stimulate vesicle fusion, the suppression of N-type channels augments dynamic range without affecting transmitter release.