The Neurobiology of Sleep–Wake Systems: An Overview

Abstract

Following studies of patients with postinfluenza encephalitis, the neuropathologist von Economo reported that inflammatory lesions of the preoptic area (POA) were often associated with insomnia and therefore proposed that the POA was critical for the production of normal sleep [1]. Then, Ranson in monkeys, Nauta in rats, and McGinty in cats showed that POA lesions induce a profound and persistent insomnia [2--4]. It was later shown in cats that POA electrical stimulation induces EEG slow-wave activity and sleep (SWS) [5]. Finally, putative sleep-promoting neurons displaying an elevated discharge rate during SWS compared to waking (W), diffusely distributed within a large region encompassing the horizontal limb of the diagonal bands of Broca and the lateral preoptic area-substantia innominata were recorded in freely moving cats [6]. Altogether, these studies indicate that the POA is a unique brain structure containing neurons that directly promote sleep.