Intraretinal analysis of the threshold dark-adapted ERG of cat retina.

1. The dark-adapted electroretinogram (ERG) obtained with 4-s flashes near threshold and at low intensities has three clear negative components: 1) a fast negative response at stimulus onset, 2) a slow negative response that increases in amplitude for about 2 s, and 3) a negative-going OFF response. The fast negative response was previously shown to originate from the scotopic threshold response (STR) arising in the proximal portion of neural retina. We investigated the intraretinal origins of the other two negative components and found that they also have origins in neural retina proximal to the photoreceptors. 2. In this study the ERG evoked in response to diffuse illumination of the dark-adapted cat retina was recorded between a chlorided silver wire in the vitreous and a plate behind the eye. Extracellular field potentials were recorded simultaneously with a microelectrode placed intraretinally at different retinal depths. In some cases light-dependent changes in extracellular K+ concentration ([K+]o) were recorded with the K+-selective barrel of a double-barreled microelectrode. 3. The three negative-going ERG potentials increased in amplitude from threshold up to approximately 6.0 log q.deg-2.s-1. The potential during illumination then became nearly flat, and the negative OFF response was exaggerated. At higher intensities, positive-going PII (DC-component and b-wave) and the c-wave emerged, whereas the a-wave (negative-going) was usually below threshold. 4. The slow negative ERG response was generated in neural retina, rather than by the retinal pigment epithelium. The response was positive-going in the transretinal recordings obtained in subretinal space. It was not, however, related to two positive-going responses from distal retina previously described as contributing negative components to the ERG: the neural retina component of the c-wave, termed slow PIII, and the rod-receptor potential. The slow negative response had a slower time course and lower threshold than slow PIII, and, more importantly, it was present in the absence of the [K+]o decrease in subretinal space that causes slow PIII. Furthermore, APB (1.2 mM vitreal concentration) blocked the entire negative-going ERG, whereas at higher intensities it blocked PII but not the c-wave in the ERG or slow PIII in transretinal recordings. These results indicate that the negative-going ERG components near threshold and at low intensities all originated proximal to the photoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)