A noncanonical inhibitory circuit dampens behavioral sensitivity to light

Author:

Sonoda Takuma12ORCID,Li Jennifer Y.1ORCID,Hayes Nikolas W.12ORCID,Chan Jonathan C.3ORCID,Okabe Yudai1ORCID,Belin Stephane4ORCID,Nawabi Homaira4ORCID,Schmidt Tiffany M.15ORCID

Affiliation:

1. Department of Neurobiology, Northwestern University, Evanston, IL, USA.

2. Northwestern University Interdepartmental Neuroscience Program, Northwestern University, Chicago, IL, USA.

3. Microsoft, Redmond, WA, USA.

4. University Grenoble Alpes, Inserm, U1216, Grenoble Institut Neurosciences, 38000 Grenoble, France.

5. Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.

Abstract

Retinal ganglion cells that release GABA Retinal ganglion cells (RGCs) communicate light signals from the retina to the brain and were previously considered to signal exclusively through release of excitatory neurotransmitters. There have been earlier hints of RGCs producing the inhibitory neurotransmitter γ-aminobutyric acid (GABA), but the specific cells have never been identified and their function was entirely unknown. Sonoda et al. found that a subpopulation of intrinsically photosensitive RGCs (ipRGCs) releases GABA (see the Perspective by Ding and Wei). Removal of GABA signaling from ipRGCs led to an increased light sensitivity of the pupillary light reflex and of circadian photoentrainment. GABA release thus moved the dynamic range of these non–image-forming behaviors to bright light intensities. These results explain why these behaviors are so much less sensitive to environmental lighting conditions than conscious visual perception. Science , this issue p. 527 ; see also p. 471

Funder

NIH Office of the Director

National Eye Institute

Alfred P. Sloan Foundation

Esther A. and Joseph Klingenstein Fund

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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