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The Journal of Neuroscience, May 1, 2003, 23(9):3649

Dynamic GABA_A Receptor Subtype-Specific Modulation of the Synchrony and Duration of Thalamic Oscillations

Vikaas S. Sohal¹, Ruth Keist², Uwe Rudolph², and John R. Huguenard¹

¹ Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, California 94305-5122, and ² Institute of Pharmacology and Toxicology, University of Zürich, CH-8057 Zürich, Switzerland

Networks of interconnected inhibitory neurons, such as the thalamic reticular nucleus (TRN), often regulate neural oscillations. Thalamic circuits generate sleep spindles and may contribute to some forms of generalized absence epilepsy, yet the exact role of inhibitory connections within the TRN remains controversial. Here, by using mutant mice in which the thalamic effects of the anti-absence drug clonazepam (CZP) are restricted to either relay or reticular nuclei, we show that the enhancement of intra-TRN inhibition is both necessary and sufficient for CZP to suppress evoked oscillations in thalamic slices. Extracellular and intracellular recordings show that CZP specifically suppresses spikes that occur during bursts of synchronous firing, and this suppression grows over the course of an oscillation, ultimately shortening that oscillation. These results not only identify a particular anatomical and molecular target for anti-absence drug design, but also elucidate a specific dynamic mechanism by which inhibitory networks control neural oscillations.

Key words: thalamus; generalized absence epilepsy; spike wave discharge; benzodiazepines; interneuronal network; inhibition

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Copyright © 2003 Society for Neuroscience  0270-6474/03/2393649-09$05.00/0

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