RESUMO
Previous studies reported that the ERG b-wave is generated by changes of membrane potential of the Müller Cell, mediated by a proximal and a distal extracellular [K+] increase. From measurements with K+ sensitive electrodes there is some evidence that the proximal K+ source is generated by amacrine cell activity. It has been shown autoradiographically that in the rabbit retina GABA is located within a subgroup of amacrine cells, in interplexiform cells and horizontal cells. The effects of GABA, picrotoxin and bicuculline on the ERG of the isolated superfused retina were investigated. Picrotoxin between 10(-4) and 10(-3) M/l and bicuculline between 10(-5) and 10(-4) M/l enhanced the a- and b-wave amplitudes. The b-wave peaked at a later time and decayed at a slower rate than did the control ERG. In higher concentrations than 10(-5) M/l GABA had the opposite effect. In experiments with isolation of the PIII by means of 10(-2) M/l Aspartate or lowering of temperature to 22 degrees C, no effect of GABA on PIII could be shown. The present investigation supports participation of GABAergic cells in b-wave generation. As an underlying mechanism a proximal K+ source is assumed, which is modified by amacrine cell activity.
