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Prakash Adhikari, Andrew J Zele, Dingcai Cao, Jan J Kremers, Beatrix K. Feigl; Melanopsin interacting with the cone-mediated white noise electroretinogram (wnERG). Invest. Ophthalmol. Vis. Sci. 2018;59(9):5037.
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© ARVO (1962-2015); The Authors (2016-present)
Melanopsin retinal ganglion cells form intra-retinal axon collaterals that are thought to provide a route for retrograde transmission from melanopsin cells via dopaminergic amacrine cells to outer retinal photoreceptors; this pathway is not well understood in humans. This study investigated how melanopsin signalling influences cone function in humans using the photopic temporal white noise electroretinogram (wnERG).
The wnERG was recorded in healthy observers (23-41 yrs) by applying a photoreceptor silent-substitution technique to independently control the melanopsin, rod and three cone photoreceptor (L-, M-, and S-cone) excitations using a 5-primary photostimulator. Observer calibrations corrected for individual differences in pre-receptoral filtering. Temporal white noise stimuli were presented in 1 s epochs containing 1024 normally distributed photoreceptor excitations (evenly distributed in the 0-64 Hz frequency range) separated by 1 ms blanks and repeated 160 times. The wnERG was recorded for: (1) rod and cone silent, melanopsin noise, (2) rod and melanopsin silent, LMS-cone noise, and (3) additive LMS + melanopsin noise. The white noise stimuli were presented in Maxwellian view (30° diameter with a 10.5° macular block) at a mean adaptation level of 1,592 cd.m-2 (80,000 Td with an 8 mm dilated pupil). The impulse response function (IRF) was derived by cross-correlation between the white noise stimulus and the wnERG.
Melanopsin isolated white noise stimuli did not elicit a measurable IRF whereas LMS-cone noise and the additive LMS-cone + melanopsin noise produced repeatable IRFs with N1 (a-wave-like) and P1 (b-wave-like) components. The combined LMS + melanopsin delayed the N1 implicit time (mean ± SEM; 29.0 ± 4.9 ms vs 23.3 ± 2.7 ms) and P1 implicit time (53.5 ± 4.7 ms vs 49.0 ± 4.0 ms) and suppressed the N1 amplitude (-2.1 ± 0.7 µV.s vs -2.8 ± 0.7 µV.s) and N1-P1 amplitude (5.9 ± 2.2 µV.s vs 10.6 ± 2.5 µV.s) relative to the LMS condition.
Melanopsin activation slows and attenuates the human cone wnERG, potentially mediated via intra-retinal melanopsin cell collaterals to dopaminergic amacrine cell dendrites. These findings may have implications for understanding the role of melanopsin in setting retinal gain control and light adaptation for encoding the ambient environmental illumination for image forming vision.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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