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Chase B Hellmer, Jeremy Bohl, Robert G Smith, Tomomi Ichinose; Investigating the Mechanisms Underlying the Starburst Amacrine Cell Light Response Polarity Switch. Invest. Ophthalmol. Vis. Sci. 2020;61(7):5061.
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© ARVO (1962-2015); The Authors (2016-present)
Starburst amacrine cells (SACs) are key neurons for retinal motion computation, communicating object motion information to postsynaptic direction selective ganglion cells (DSGCs). It has recently been shown that after visual adaptation anatomically ON-SACs respond with a physiological OFF response. While the underlying mechanisms are unclear, it has been suggested that a unique cone-rod crossover inhibition effect may lead to loss of glutamate during the light ON period. SACs have also been shown to express multiple inhibitory potassium channel types. We sought to investigate the mechanisms underlying this phenomenon.
Patch clamp recordings were conducted from ON-SACs in C57BL6/J or Chat-Cre/Ai9 mice. Current and voltage clamp experiments were carried out using light steps or moving bars at mesopic to photopic light levels at 40-100% Weber contrast. Additionally, 20mM HEPES was perfused in the bath to block horizontal cell feedback. To block Kv3 channels in ON-SACs, we applied TEA in the bath (1mM) or in the intracellular solution (10 mM). ECl and EK were set to -60mV and -90mV for voltage clamp analysis.
In response to a step light stimulation, 52% of ON-SACs hyperpolarized instead of depolarizing (14/27 SACs). In these SACs, moving stimuli of both centripetal and centrifugal directions also hyperpolarized the cells, and polarity switching frequently happened during the recording. Horizontal cells may cause rod-cone crossover inhibition to suppress cone bipolar cell glutamate release. Therefore, we blocked horizontal cell feedback by applying HEPES in the bath, which appeared to reverse the polarity switch back to ON responses in 2 out of 6 hyperpolarizing ON SACs. In addition, we applied TEA to block Kv3 channels, which did not change the hyperpolarization. Voltage clamp analysis of these cells revealed the presence of both transient and sustained K+ currents, but Cl- currents did not contribute to the hyperpolarization.
The mechanisms underlying SAC polarity switch have yet to be revealed. Our studies show that a combination of horizontal cell mediated cone-rod crossover inhibition and activation of strong potassium currents may provide the mechanism for this effect. One interesting possibility for such a modulation of potassium channels may be a GABA-b mechanism.
This is a 2020 ARVO Annual Meeting abstract.
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