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• W1570757432 abstract "Correspondence should be addressed to E.S.B. (esb@media.mit.edu). 12These authors contributed equally to this work. Accession codes. GenBank: KM000925, KM000926, KM000927 and KM000928. Note: Any Supplementary Information and Source Data files are available in the online version of the paper. AUTHOR CONTRIBUTIONS A.S.C. and E.S.B. coordinated all experiments and data analysis. A.S.C. designed and developed Jaws and cloned all constructs. A.S.C. performed in vivo glass pipette extracellular recordings and in vitro electrophysiology. M.L.M. and J.A.C. performed in vivo tetrode extracellular recordings. V.B. performed in vivo multielectrode array recordings. A.S.C., G.A.C.M., A.T.S. and A.Y. performed slice electrophysiology. A.S.C., M.L.M., G.A.C.M., A.T.S., J.A.C., V.B. and M.O. performed in vivo viral injections. A.S.C., M.L.M., V.B., G.A.C.M., A.T.S., S.B.R. and M.O. performed histological processing and fluorescence imaging. S.B.K. and C.R.F. designed or performed autopatch experiments. A.S.C. and N.C.K. performed transfections, cell culture and in vitro viral infections. M.A.H. conducted Monte Carlo modeling. L.C.A. carried out light propagation measurements. R.C.B. and B.D.A. carried out X-ray scans to measure mouse skull thicknesses for the Monte Carlo model. A.S.C., M.L.M., V.B., G.A.C.M., A.T.S., B.Y.C., X.H., J.A.C., B.R. and E.S.B. contributed to study design and data interpretation. J.A.C., B.R., K.M.T., Y.L. and E.S.B. supervised all aspects of the work. A.S.C. and E.S.B. wrote the paper with contributions from the other authors. COMPETING FINANCIAL INTERESTS The authors declare competing financial interests: details are available in the online version of the paper. Reprints and permissions information is available online at http://www.nature.com/reprints/index.html A Supplementary Methods Checklist is available. NIH Public Access Author Manuscript Nat Neurosci. Author manuscript; available in PMC 2014 October 03. Published in final edited form as: Nat Neurosci. 2014 August ; 17(8): 1123–1129. doi:10.1038/nn.3752. N IH -P A A uhor M anscript N IH -P A A uhor M anscript N IH -P A A uhor M anscript Optogenetic inhibition of the electrical activity of neurons enables the causal assessment of their contributions to brain functions. Red light penetrates deeper into tissue than other visible wavelengths. We present a red-shifted cruxhalorhodopsin, Jaws, derived from Haloarcula (Halobacterium) salinarum (strain Shark) and engineered to result in red light–induced photocurrents three times those of earlier silencers. Jaws exhibits robust inhibition of sensoryevoked neural activity in the cortex and results in strong light responses when used in retinas of retinitis pigmentosa model mice. We also demonstrate that Jaws can noninvasively mediate transcranial optical inhibition of neurons deep in the brains of awake mice. The noninvasive optogenetic inhibition opened up by Jaws enables a variety of important neuroscience experiments and offers a powerful general-use chloride pump for basic and applied neuroscience. Optogenetic inhibition, the use of light-activated ion pumps to enable transient activity suppression of genetically targeted neurons by pulses of light1–3, is valuable for the causal parsing of neural circuit component contributions to brain functions and behaviors. A major limit to the utility of optogenetic inhibition is the addressable quantity of neural tissue. Previous optogenetic hyperpolarizing proton pumps (Arch1, ArchT3, Mac1) and chloride pumps (eNpHR4, eNpHR3.0 (ref. 2)) have successfully inhibited volumes of approximately a cubic millimeter, but many neuroscience questions require the ability to suppress larger tissue volumes. A number of pharmacogenetic, chemical and genetic strategies have been used for this purpose5–7, but it would ideally be possible to address these large brain volumes with the millisecond temporal precision of optogenetic tools. Another common desire in optogenetic experiments is to minimize invasiveness from inserting optical fibers into the brain, which displaces brain tissue and can lead to side effects such as brain lesion, neural morphology changes, glial inflammation and motility, or compromise of asepsis8–10. Less invasive strategies that do not require an implanted optical device would also increase experimental convenience and enable longer timescale experiments than often feasible with fragile implants. While a number of previous studies using channelrhodopsins have attempted to address this problem11–16, noninvasive optical inhibition has not yet been possible. To enable noninvasive large-volume optogenetic inhibition, we engineered and characterized Jaws, a spectrally shifted cruxhalorhodopsin derived from the species H. salinarum (strain Shark)17, which mediates strong red light–driven neural inhibition. Jaws is capable of powerful optical hyperpolarization in a variety of neuroscientific contexts: it successfully enabled suppression of visually evoked neural activity in mice, functioned in cone photoreceptors to restore greater light sensitivity in mouse models than possible with previous opsins and enabled the noninvasive transcranial inhibition of neurons in brain structures up to 3 mm deep. This new reagent thus makes a variety of important experiments amenable to optogenetic investigation. Chuong et al. Page 2 Nat Neurosci. Author manuscript; available in PMC 2014 October 03. N IH -P A A uhor M anscript N IH -P A A uhor M anscript N IH -P A A uhor M anscript" @default.
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• W1570757432 date "2014-07-06" @default.
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• W1570757432 title "Noninvasive optical inhibition with a red-shifted microbial rhodopsin" @default.
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