Contribution of rod, on-bipolar, and horizontal cell light responses to the ERG of dogfish retina

Simultaneous extracellular ERG and intracellular recordings from horizontal and ON-bipolar cells were obtained from the dark-adapted retina of the dog fish. The light intensity-peak response relation (IR) and time course of on -bipolar cell responses closely resembled that of the ERG b-wave, but only at low light intensities [<10 rhodopsin molecules bleached per rod (Rh*)]. Block of on-bipolar cell responses with 50 mu M 2-amino-4-phosphonobutyrate (APB) abolished the b-wave and unmasked a vitreal-negative wave. Subtracti on from the control ERG resulted in the isolation of a vitreal-positive ERG with an IR which matched that of on-bipolar calls over the full range of l ight intensities. The D.C. component of the ERG arises as a result of susta ined depolarization of on-bipolar cells in response to long (>0.5 s) dim li ght stimuli, or following bright light flashes. The IR of horizontal cells and the vitreal-negative wave unmasked by APE could be matched by scaling a t low light intensities (<5 Rh*). However, horizontal cell responses satura ted at about 30 Rh*, while the vitreal-negative wave continued to increase in amplitude. The time course of horizontal cell membrane current with dim flashes could be matched to the rising phase of the vitreal-negative wave, assuming that the delay in generating the voltage response in horizontal ce lls is due to their longs (100 ms) membrane Lime constant. Blocking post-ph otoreceptor activity resulted in a much smaller vitreal-negative wave than that unmasked by APB alone. We conclude that the b-wave arises from on-bipo lar cell depolarization, while the leading edge of the a-wave is a composit e of the change in extracellular voltage drop across the rod layer and a co mponent (proximal PIII) reflecting a decrease in extracellular K+ as horizo ntal cell synaptic channels close with light.