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J.M. Ackert, I. Perlman, J. Lee, S. Bloomfield; Pharmacology of the ON Direction Selective Ganglion Cells in the Rabbit Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2336.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine the circuitry underlying the synchrony between neighboring ON direction selective (ON–DS) ganglion cells and the inhibition and latency changes associated with null direction stimulation. Methods: Dual, simultaneous extracellular recordings were obtained from pairs of ON–DS cells visualized with transcleral infrared illumination in a flattened retinal preparation of the albino rabbit. Results: We reported at the last ARVO meeting that neighboring ON–DS cells normally show synchronized spike activity. However, null direction stimulation results in: (1) a reduction in discharge frequency; (2) a shift in the latency of firing; and (3) a desynchronization of the activity of neighboring ON–DS cells. To determine if the coupling we have described between neighboring ON–DS cells via amacrine cells underlies their synchronous spiking, we examined the effects of the gap junction blocker 14–beta–glycyrrhetinic acid (14–GA). Application of 14–GA significantly reduced or abolished the synchrony between neighboring ON–DS cells. Interestingly, we found that 14–GA also reduced their direction selectivity. To determine whether the reduced spike activity, desynchronization, and latency shift associated with null stimulation were due to a GABAergic inhibition, we examined the effects of the GABA receptor blocker picrotoxin. Application of picrotoxin resulted in a complete loss of direction selectivity of ON–DS cells associated with increased responses to both preferred and null direction stimulation. Moreover, the latency shift and desynchronization were blocked by picrotoxin, resulting in synchronous activity between neighboring ON–DS cells for both preferred and null stimulation. Conclusions: Our results indicate that the coupling between ON–DS and amacrine cells underlies the synchronous activity between neighboring ON–DS cells. Further, null direction stimulation results in a GABAergic inhibition that gives rise to a reduced firing rate, a latency shift, and a desynchronization of the activity of neighboring ON–DS cells. Thus, our results suggest that null stimulation will result in not just an attenuated signal transmitted to the accessory optic tract, but a reduction in temporal summation due to signal desynchrony.
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