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The Journal of Neuroscience, July 13, 2005, 25(28):6716-6720; doi:10.1523/JNEUROSCI.1887-05.2005

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BRIEF COMMUNICATION
Discharge of Identified Orexin/Hypocretin Neurons across the Sleep-Waking Cycle

Maan Gee Lee,1,2 * Oum K. Hassani,1 * and Barbara E. Jones1

1Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4, and 2Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, South Korea

Although maintained by multiple arousal systems, wakefulness falters if orexin (hypocretin), orexin receptors, or orexin neurons are deficient; narcolepsy results with hypersomnolence or sudden onset of rapid eye movement sleep [or paradoxical sleep (PS)] and loss of muscle tonus. To learn how orexin neurons maintain wakefulness, we recorded neurons in head-fixed rats across the sleep-waking cycle and then labeled them with Neurobiotin to identify them by immunohistochemistry. We show that identified orexin neurons discharge during active waking, when postural muscle tone is high in association with movement, decrease discharge during quiet waking in absence of movement, and virtually cease firing during sleep, when postural muscle tone is low or absent. During PS, they remain relatively silent in association with postural muscle atonia and most often despite phasic muscular twitches. They increase firing before the end of PS and thereby herald by several seconds the return of waking and muscle tone. The orexin neurons would thus stimulate arousal, while antagonizing sleep and muscle atonia.

Key words: arousal; hypothalamus; sleep; narcolepsy; hypocretin; REMS

Received May 11, 2005; revised June 9, 2005; accepted June 10, 2005.




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