Driving fast-spiking cells induces gamma rhythm and controls sensory responses

Jessica A. Cardin, Marie Carlén, Konstantinos Meletis, Ulf Knoblich, Feng Zhang, Karl Deisseroth (), Li-Huei Tsai () and Christopher I. Moore ()
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Jessica A. Cardin: MIT, Cambridge, Massachusetts 02139, USA
Marie Carlén: Picower Institute for Learning and Memory, MIT, Cambridge, Massachusetts 02139, USA
Konstantinos Meletis: Picower Institute for Learning and Memory, MIT, Cambridge, Massachusetts 02139, USA
Ulf Knoblich: MIT, Cambridge, Massachusetts 02139, USA
Feng Zhang: Stanford University, Stanford, California 94305, USA
Karl Deisseroth: Stanford University, Stanford, California 94305, USA
Li-Huei Tsai: Picower Institute for Learning and Memory, MIT, Cambridge, Massachusetts 02139, USA
Christopher I. Moore: MIT, Cambridge, Massachusetts 02139, USA

Nature, 2009, vol. 459, issue 7247, 663-667

Abstract: Abstract Cortical gamma oscillations (20-80 Hz) predict increases in focused attention, and failure in gamma regulation is a hallmark of neurological and psychiatric disease. Current theory predicts that gamma oscillations are generated by synchronous activity of fast-spiking inhibitory interneurons, with the resulting rhythmic inhibition producing neural ensemble synchrony by generating a narrow window for effective excitation. We causally tested these hypotheses in barrel cortex in vivo by targeting optogenetic manipulation selectively to fast-spiking interneurons. Here we show that light-driven activation of fast-spiking interneurons at varied frequencies (8-200 Hz) selectively amplifies gamma oscillations. In contrast, pyramidal neuron activation amplifies only lower frequency oscillations, a cell-type-specific double dissociation. We found that the timing of a sensory input relative to a gamma cycle determined the amplitude and precision of evoked responses. Our data directly support the fast-spiking-gamma hypothesis and provide the first causal evidence that distinct network activity states can be induced in vivo by cell-type-specific activation.

Date: 2009
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DOI: 10.1038/nature08002

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