Purchase this article with an account.
Aaron N. Reifler, Andrew P. Chervenak, Michael E. Dolikian, Brian A. Benenati, Benjamin Y. Li, Rebecca D. Wachter, Andrew M. Lynch, Zachary D. Demertzis, Benjamin S. Meyers, Kwoon Y Wong; Spiking, sustained ON amacrine cells receive input from intrinsically photosensitive retinal ganglion cells (ipRGCs) through gap junctions. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5867.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
We previously reported that sustained dopaminergic amacrine cells receive input from ipRGCs via AMPA/kainate receptors (Zhang et al. PNAS 2008). Here, we tested the hypothesis that ipRGCs signal to additional sustained ON amacrine cells.
We whole-cell-recorded from >2,000 displaced amacrine cells in Ames-superfused rat eyecups and presented 10-sec light steps to find cells that depolarized for the duration of the light. Recorded cells were dye-filled and imaged using confocal microscopy. To quantify the sustainedness of a photoresponse, we measured peak amplitude and the amplitude near the end of the light step, and divided the latter by the former to calculate the final-to-peak amplitude ratio.
193 displaced amacrine cells had sustained ON photoresponses. 40 of these were non-spiking and their light responses were abolished when rod/cone input was blocked by the glutamate analogs L-AP4, DNQX and D-AP5. The other 153 cells spiked and showed sluggish photoresponses during rod/cone block with a λmax near that for melanopsin, suggesting non-glutamatergic input from ipRGCs. These ipRGC-driven amacrines comprised 5 morphological types that either monostratified in S5 of the inner plexiform layer, or bistratified in S1 and S5. Using Weiler and colleagues’ nomenclature (Mueller et al. J. Comp. Neurol. 2007), these cell types were PA-S5 (polyaxonal), MA-S5 (medium-field), MA-S1/S5, WA-S5 (wide-field), and WA-S1/S5. The photoresponses evoked during rod/cone block were little changed by TTX or GABA/glycine receptor antagonists, but were abolished by the gap junction blocker meclofenamic acid (MFA). When MFA was added to normal Ames (which permitted rod/cone signaling), these amacrines’ light responses became less tonic, reducing the final-to-peak amplitude ratio from 0.51 to 0.37 (p<0.05).
All spiking sustained ON displaced amacrine cells receive ipRGC input. Unlike the dopaminergic amacrine cells which receive TTX-sensitive glutamatergic input from ipRGCs’ axon collaterals (Atkinson & Zhang ARVO 2014; Yeh & Chen SfN 2014), these displaced amacrines are electrically coupled to ipRGCs. Such coupling could be mediated by dendrodendritic gap junctions because these cells stratify in S1 and S5 just like ipRGCs. The sustained quality of these amacrines’ light responses is due to both ipRGC input and conventional rod/cone input.
This PDF is available to Subscribers Only