Abstract
SummaryThe detection of visual motion is a fundamental function of the visual system. How motion speed and direction are computed together at the cellular level, however, remains largely unknown. Here, we suggest a circuit mechanism by which excitatory inputs to direction-selective ganglion cells in the mouse retina become sensitive to the motion speed and direction of image motion. Electrophysiological, imaging, and connectomic analyses provide evidence that the dendrites of ON direction-selective cells receive spatially offset and asymmetrically filtered glutamatergic inputs along motion-preference axis from asymmetrically wired bipolar and amacrine cell types with distinct release dynamics. A computational model shows that, with this spatiotemporal structure, the input amplitude becomes sensitive to speed and direction by a preferred direction enhancement mechanism. Our results highlight the role of an excitatory mechanism in retinal motion computation by which feature selectivity emerges from non-selective inputs.
Highlights
The retina is the first stage in the mammalian nervous system in which visual motion is computed
The detection of visual motion is a fundamental function of the visual system
We suggest a circuit mechanism by which excitatory inputs to direction-selective ganglion cells in the mouse retina become sensitive to the motion speed and direction of image motion
Summary
The retina is the first stage in the mammalian nervous system in which visual motion is computed. Retinal direction-selective (DS) cells preferentially show spiking responses to visual stimuli moving in a particular direction (preferred direction) and show less spiking to the opposite, null direction [1]. It has been suggested that a key mechanism underlying retinal direction selectivity is null-direction suppression in DS cells implemented by spatially offset and DS GABAergic inhibitory inputs from starburst amacrine cells (SACs) [2,3,4]. Later studies with glutamate imaging from the inner plexiform layer or calcium imaging from bipolar cell axon terminals have suggested that individual glutamatergic synaptic inputs are not directionally tuned [10,11,12], favoring the hypothesis of voltage clamping artifact (but see [13])
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