Neocortical excitation/inhibition balance in information processing and social dysfunction

Ofer Yizhar (), Lief E. Fenno, Matthias Prigge, Franziska Schneider, Thomas J. Davidson, Daniel J. O’Shea, Vikaas S. Sohal, Inbal Goshen, Joel Finkelstein, Jeanne T. Paz, Katja Stehfest, Roman Fudim, Charu Ramakrishnan, John R. Huguenard, Peter Hegemann () and Karl Deisseroth ()
Additional contact information
Ofer Yizhar: W083 Clark Center, 318 Campus Drive West, Stanford University
Lief E. Fenno: W083 Clark Center, 318 Campus Drive West, Stanford University
Matthias Prigge: Institute of Biology, Experimental Biophysics, Humboldt-Universität, Invalidenstraße 42
Franziska Schneider: Institute of Biology, Experimental Biophysics, Humboldt-Universität, Invalidenstraße 42
Thomas J. Davidson: W083 Clark Center, 318 Campus Drive West, Stanford University
Daniel J. O’Shea: W083 Clark Center, 318 Campus Drive West, Stanford University
Vikaas S. Sohal: W083 Clark Center, 318 Campus Drive West, Stanford University
Inbal Goshen: W083 Clark Center, 318 Campus Drive West, Stanford University
Joel Finkelstein: W083 Clark Center, 318 Campus Drive West, Stanford University
Jeanne T. Paz: W083 Clark Center, 318 Campus Drive West, Stanford University
Katja Stehfest: Institute of Biology, Experimental Biophysics, Humboldt-Universität, Invalidenstraße 42
Roman Fudim: Institute of Biology, Experimental Biophysics, Humboldt-Universität, Invalidenstraße 42
Charu Ramakrishnan: W083 Clark Center, 318 Campus Drive West, Stanford University
John R. Huguenard: W083 Clark Center, 318 Campus Drive West, Stanford University
Peter Hegemann: Institute of Biology, Experimental Biophysics, Humboldt-Universität, Invalidenstraße 42
Karl Deisseroth: W083 Clark Center, 318 Campus Drive West, Stanford University

Nature, 2011, vol. 477, issue 7363, 171-178

Abstract: Abstract Severe behavioural deficits in psychiatric diseases such as autism and schizophrenia have been hypothesized to arise from elevations in the cellular balance of excitation and inhibition (E/I balance) within neural microcircuitry. This hypothesis could unify diverse streams of pathophysiological and genetic evidence, but has not been susceptible to direct testing. Here we design and use several novel optogenetic tools to causally investigate the cellular E/I balance hypothesis in freely moving mammals, and explore the associated circuit physiology. Elevation, but not reduction, of cellular E/I balance within the mouse medial prefrontal cortex was found to elicit a profound impairment in cellular information processing, associated with specific behavioural impairments and increased high-frequency power in the 30–80 Hz range, which have both been observed in clinical conditions in humans. Consistent with the E/I balance hypothesis, compensatory elevation of inhibitory cell excitability partially rescued social deficits caused by E/I balance elevation. These results provide support for the elevated cellular E/I balance hypothesis of severe neuropsychiatric disease-related symptoms.

Date: 2011
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DOI: 10.1038/nature10360

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