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This article is part of the Research Topic Genetic techniques and circuit analysis

Review ARTICLE

Front. Mol. Neurosci., 20 January 2010 | http://dx.doi.org/10.3389/neuro.02.031.2009

Optogenetic deconstruction of sleep–wake circuitry in the brain

Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA, USA
How does the brain regulate the sleep–wake cycle? What are the temporal codes of sleep- and wake-promoting neural circuits? How do these circuits interact with each other across the light/ dark cycle? Over the past few decades, many studies from a variety of disciplines have made substantial progress in answering these fundamental questions. For example, neurobiologists and basal forebrain. Sleep-promoting circuits have been found in the preoptic area and hypothalamus. One of the greatest challenges in recent years has been to selectively record and manipulate these sleep–wake centers in vivo with high spatial and temporal resolution. Recent developments in microbial opsin-based neuromodulation tools, collectively referred to as “optogenetics,” have provided a novel method to demonstrate causal links between neural activity and specifi c behaviors. Here, we propose to use optogenetics as a fundamental tool to probe the necessity, suffi ciency, and connectivity of defi ned neural circuits in the regulation of sleep and wakefulness.
Keywords:
hypothalamus, sleep, wakefulness, optogenetics, hypocretins/orexins
Citation:
Adamantidis A, Carter MC and de Lecea L (2010). Optogenetic deconstruction of sleep–wake circuitry in the brain. Front. Mol. Neurosci. 2:31. doi: 10.3389/neuro.02.031.2009
Received:
31 August 2009;
 Paper pending published:
12 September 2009;
Accepted:
18 December 2009;
 Published online:
20 January 2010.

Edited by:

William Wisden, Imperial College, UK

Reviewed by:

Scott Sternson, Howard Hughes Medical Institute, USA
Patrice Fort, Centre National de la Recherche Scientifique, France
William Wisden, Imperial College, UK
Copyright:
© 2010 Adamantidis, Carter and de Lecea. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence:
Antoine Adamantidis and Luis de Lecea, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 701 B Welch Road, Palo Alto, CA 94304, USA. e-mail: tidis@stanford.edu; llecea@stanford.edu