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Silvia Park, Bart Borghuis, In-Jung Kim, Loren Looger, Jonathan Demb; Direction tuning of bipolar cell glutamate release onto direction-selective ganglion cells in mouse retina. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1297.
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© ARVO (1962-2015); The Authors (2016-present)
Direction selective ganglion cells (DSGCs) fire strongly to motion in a preferred direction and weakly to motion in the opposite, null direction. One established mechanism for this direction selectivity is asymmetric GABA release from presynaptic starburst amacrine cell dendrites. A second postulated mechanism for direction selectivity is asymmetric glutamate release from presynaptic bipolar cell terminals. Here, we tested this second mechanism with direct optical measurements of glutamate release onto DSGC dendrites.
Spike responses and whole-cell currents were recorded from ON-OFF DSGCs in wild type and transgenic mouse retinas (DRD4 and BD lines). DS responses were elicited by either a drifting grating or a moving spot. We used two-photon imaging to target GFP-expressing DSGCs and to monitor glutamate release with a genetically encoded glutamate sensor protein expressed in their dendrites (iGluSnFR; Marvin et al., 2013).
The preferred and null axis of DSGCs was determined from the spike responses. ON-OFF DSGCs showed directionally asymmetric excitatory (EPSCs) and inhibitory postsynaptic currents (IPSCs): EPSCs were largest in the preferred direction, while IPSCs were largest in the null direction. The direction selectivity in EPSCs persisted in the presence of a nicotinic acetylcholine receptor antagonist (hexamethonium), consistent with the proposed DS of glutamatergic input from bipolar cells. However, we found no difference in iGluSnFR responses (fractional change in fluorescence) to preferred and null directions (0.21+0.09; 0.20+0.08, n=4 cells).
The apparent direction tuning of EPSCs was not confirmed by direct optical measurements of glutamate release onto DSGC dendrites. It has been suggested that apparent direction tuning in glutamate release may reflect an artifact of whole-cell recording associated with incomplete voltage clamp in the presence of strong inhibition during null-direction motion (Poleg-Polsky and Diamond, 2011). Our data are consistent with this interpretation and suggest that bipolar cell glutamate release is not direction-tuned.
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