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Targeting light-gated chloride channels to neuronal somatodendritic domain reduces their excitatory effect in the axon

View ORCID ProfileJessica E. Messier, Hongmei Chen, View ORCID ProfileZhao-Lin Cai, Mingshan Xue
doi: https://doi.org/10.1101/331165
Jessica E. Messier
1Department of Neuroscience, Baylor College of Medicine, Houston Texas, 77030, USA
3The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, Houston Texas, 77030, USA
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  • ORCID record for Jessica E. Messier
Hongmei Chen
1Department of Neuroscience, Baylor College of Medicine, Houston Texas, 77030, USA
3The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, Houston Texas, 77030, USA
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Zhao-Lin Cai
1Department of Neuroscience, Baylor College of Medicine, Houston Texas, 77030, USA
3The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, Houston Texas, 77030, USA
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Mingshan Xue
1Department of Neuroscience, Baylor College of Medicine, Houston Texas, 77030, USA
2Department of Molecular and Human Genetics, Baylor College of Medicine, Houston Texas, 77030, USA
3The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, Houston Texas, 77030, USA
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  • For correspondence: mxue@bcm.edu
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Abstract

Light-gated chloride channels are emerging as promising optogenetic tools for inhibition of neural activity. However, their effects depend on the transmembrane chloride electrochemical gradient and may be complex due to the heterogeneity of this gradient in different developmental stages, neuronal types, and subcellular compartments. Here we characterized a light-gated chloride channel, GtACR2, in mouse cortical neurons. We found that GtACR2 activation inhibited the soma, but unexpectedly depolarized the presynaptic terminals resulting in neurotransmitter release. Other light-gated chloride channels had similar effects. Reducing the chloride concentrations in the axon and presynaptic terminals diminished the GtACR2-induced neurotransmitter release, indicating an excitatory effect of chloride channels in these compartments. A novel hybrid somatodendritic targeting motif reduced the GtACR2-induced neurotransmitter release while enhancing the somatic photocurrents. Our results highlight the necessity of precisely determining the effects of light-gated chloride channels under specific experimental conditions and provide a much-improved light-gated chloride channel for optogenetic inhibition.

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Posted May 25, 2018.
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Targeting light-gated chloride channels to neuronal somatodendritic domain reduces their excitatory effect in the axon
Jessica E. Messier, Hongmei Chen, Zhao-Lin Cai, Mingshan Xue
bioRxiv 331165; doi: https://doi.org/10.1101/331165
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Targeting light-gated chloride channels to neuronal somatodendritic domain reduces their excitatory effect in the axon
Jessica E. Messier, Hongmei Chen, Zhao-Lin Cai, Mingshan Xue
bioRxiv 331165; doi: https://doi.org/10.1101/331165

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