Abstract
1. The actions of two pharmacological agents, barium ions (Ba2+) and picrotoxin (PTX), were examined on components of the electroretinogram (ERG) in frog retina. Depth profiles of light-evoked field potentials were recorded, and current source densities (CSDs) were computed from these. 2. Ba2+ abolished the M-wave, slow PIII, and the c-wave, but only decreased b-wave amplitude down to approximately 65% of control amplitude. 3. Ba2+ abolished a slow current sink in the inner plexiform layer (IPL) and the source at the inner limiting membrane (ILM). This IPL sink/ILM source appears to generate the M-wave. 4. Ba2+ decreased the current sink at the outer plexiform layer (OPL) to approximately 70% of control amplitude, and it increased an IPL source. This Ba(2+)-resistant OPL sink/IPL source appears to generate a significant portion of the b-wave. The Ba(2+)-sensitive portion of the b-wave might be generated by Müller cells. 5. PTX enhanced retinal field potentials, particularly the M-wave in the proximal retina. This enhanced M-wave was shown to originate from an enhanced IPL sink/ILM source. 6. Our results suggest that the M-wave originates from Müller cells, through the spatial buffering of the light-evoked increase in [K+]o of the proximal retina. A portion of the b-wave may also originate from Müller cells, but a stronger direct contribution from depolarizing bipolar cells is suggested.
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