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Causal evidence for retina-dependent and -independent visual motion computations in mouse cortex.


ABSTRACT: How neuronal computations in the sensory periphery contribute to computations in the cortex is not well understood. We examined this question in the context of visual-motion processing in the retina and primary visual cortex (V1) of mice. We disrupted retinal direction selectivity, either exclusively along the horizontal axis using FRMD7 mutants or along all directions by ablating starburst amacrine cells, and monitored neuronal activity in layer 2/3 of V1 during stimulation with visual motion. In control mice, we found an over-representation of cortical cells preferring posterior visual motion, the dominant motion direction an animal experiences when it moves forward. In mice with disrupted retinal direction selectivity, the over-representation of posterior-motion-preferring cortical cells disappeared, and their responses at higher stimulus speeds were reduced. This work reveals the existence of two functionally distinct, sensory-periphery-dependent and -independent computations of visual motion in the cortex.

SUBMITTER: Hillier D 

PROVIDER: S-EPMC5490790 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Causal evidence for retina-dependent and -independent visual motion computations in mouse cortex.

Hillier Daniel D   Fiscella Michele M   Drinnenberg Antonia A   Trenholm Stuart S   Rompani Santiago B SB   Raics Zoltan Z   Katona Gergely G   Juettner Josephine J   Hierlemann Andreas A   Rozsa Balazs B   Roska Botond B  

Nature neuroscience 20170522 7


How neuronal computations in the sensory periphery contribute to computations in the cortex is not well understood. We examined this question in the context of visual-motion processing in the retina and primary visual cortex (V1) of mice. We disrupted retinal direction selectivity, either exclusively along the horizontal axis using FRMD7 mutants or along all directions by ablating starburst amacrine cells, and monitored neuronal activity in layer 2/3 of V1 during stimulation with visual motion.  ...[more]

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