Format

Send to

Choose Destination
Nature. 2017 Feb 23;542(7642):439-444. doi: 10.1038/nature21394. Epub 2017 Feb 8.

Inhibition decorrelates visual feature representations in the inner retina.

Franke K1,2,3,4, Berens P1,2,3, Schubert T1,3, Bethge M1,2,5,6, Euler T1,2,3, Baden T1,2,3,7.

Author information

1
Centre for Integrative Neuroscience, University of Tübingen, Tübingen, Germany.
2
Bernstein Centre for Computational Neuroscience, University of Tübingen, Tübingen, Germany.
3
Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany.
4
Graduate School of Neural &Behavioural Sciences, International Max Planck Research School, University of Tübingen, Tübingen, Germany.
5
Institute for Theoretical Physics, University of Tübingen, Tübingen, Germany.
6
Max Planck Institute of Biological Cybernetics, Tübingen, Germany.
7
School of Life Sciences, University of Sussex, Brighton, UK.

Abstract

The retina extracts visual features for transmission to the brain. Different types of bipolar cell split the photoreceptor input into parallel channels and provide the excitatory drive for downstream visual circuits. Mouse bipolar cell types have been described at great anatomical and genetic detail, but a similarly deep understanding of their functional diversity is lacking. Here, by imaging light-driven glutamate release from more than 13,000 bipolar cell axon terminals in the intact retina, we show that bipolar cell functional diversity is generated by the interplay of dendritic excitatory inputs and axonal inhibitory inputs. The resulting centre and surround components of bipolar cell receptive fields interact to decorrelate bipolar cell output in the spatial and temporal domains. Our findings highlight the importance of inhibitory circuits in generating functionally diverse excitatory pathways and suggest that decorrelation of parallel visual pathways begins as early as the second synapse of the mouse visual system.

PMID:
28178238
PMCID:
PMC5325673
DOI:
10.1038/nature21394
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center