GABAc feedback pathway modulates the amplitude and kinetics of ERG b-wave in a mammalian retina in vivo

Abstract

The electroretinogram b-wave is generally believed to reflect mainly light-induced activity of ON-center bipolar cells and Muller cells. Recently, there is increasing evidence that third-order retinal neurons can also contribute significantly to the b-wave. In a previous study (Vis. Res. 40 (2000) 579) we proposed that the GABAc feedback from amacrine cells to bipolar cells can affect both the amplitude and kinetics of the b-wave. Here we show that blocking this feedback has profound effects on b-wave amplitude and kinetics. These results demonstrate that feedback to bipolar cells is an important mechanism through which amacrine cells contribute to b-wave generation. Our results also provide functional evidence that the feedback may be involved in temporal processing in the mammalian retina.