PURPOSE. To clarify the origins of the variations with retinal location of the oscillatory potentials (OPs) in the human photopic electroretinogram (ERG), inner retinal spiking and nonspiking activity was blocked pharmacologically in monkeys.
METHOD. Multifocal (mf) ERGs were recorded between DTL electrodes on the 2 eyes from 5 normal human subjects and 10 anesthetized adult monkeys (Macaca mulatta). The stimulus display consisted of 103 equal sized hexagons, within 170 of the fovea. The mfERG sequence was slowed such that presentation of each 5.3 or 2.7 cd-s/m2 hexagon was separated by at least 100 ms. The slow sequence allowed extraction of traditional OPs (90-300 Hz). Recordings in monkeys were obtained before and after intravitreal injections of TTX (4.8-7.6uM vitreal conc.) to block Na+-dependent action potentials in ganglion and amacrine cells, glutamate agonist NMDA (1.4-6.4mM) or inhibitory neurotransmitter GABA (37-55mM) to block inner retinal activity, and picrotoxin (PTX; 0.14-0.4mM) to block GABAA&C receptors.
RESULTS. The OPs present in mfERGs of humans and monkeys showed similar timing, and in both species were largest in the temporal portion of the macular region. In monkeys the nasotemporal asymmetry was removed and OPs were diminished, but not eliminated, by TTX (n=2), which also removed Sutter & Bearse’s optic nerve head component (OHNC) in these animals. OPs that were still present after TTX+NMDA (n=6) were reduced by PTX (n=3); OPs also were eliminated by GABA alone (n=2).
CONCLUSIONS. OPs in the photopic ERG originate from both spiking and nonspiking inner retinal activity. Our findings are consistent with the suggestion that the spike-driven nasotemporal OP variation reflects the ONHC of the mfERG.