Neuroanatomy and neurochemistry of sleep

Abstract

Sleep is regulated by homeostatic and circadian factors, and the regulation of sleep of mammals shares many molecular properties with the rest state of submammalian species. Several brain structures take part in waking: the basal forebrain, posterior and lateral hypothalamus, and nuclei in the tegmentum and pons. Active sleep mechanisms are located to the preoptic/anterior hypothalamic area. In addition to acetylcholine and monoamines, glutamate and hypocretin/orexin are important waking factors. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. Adenosine is an important homeostatic sleep factor acting in basal forebrain and preoptic areas through A1 and A2A receptors. Prolonged waking activates inducible nitric oxide synthase in the basal forebrain, which through energy depletion causes adenosine release and recovery sleep. Numerous genes have been found differentially displayed in waking compared with sleep, and they relate to neural transmission, synaptic plasticity, energy metabolism and stress protection. The genetic background of a few sleep disorders has been solved.

Intra-accumbens injections of the adenosine A2A agonist CGS 21680 affect effort-related choice behavior in rats

“…One of the likely explanations is that systemic administration of an adenosine A 2A agonist such as CGS 21680 produces sedation (i.e., drowsiness). The sedative effects of adenosine have been well characterized (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Systemic or intraventricular injections of adenosine, as well as local infusions into the basal forebrain, have been shown to induce sleep (Stenberg 2007).…”

“…The sedative effects of adenosine have been well characterized (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Systemic or intraventricular injections of adenosine, as well as local infusions into the basal forebrain, have been shown to induce sleep (Stenberg 2007). Sleep deprivation is associated with increases in the extracellular levels of adenosine, and non-selective adenosine antagonists such as caffeine are used to enhance wakefulness (Stenberg 2007).…”

“…Systemic or intraventricular injections of adenosine, as well as local infusions into the basal forebrain, have been shown to induce sleep (Stenberg 2007). Sleep deprivation is associated with increases in the extracellular levels of adenosine, and non-selective adenosine antagonists such as caffeine are used to enhance wakefulness (Stenberg 2007). Evidence indicates that both adenosine A 1 and A 2A receptors are involved in the regulation of sleep, though probably through different mechanisms and distinct brain areas (Stenberg 2007).…”

“…Sleep deprivation is associated with increases in the extracellular levels of adenosine, and non-selective adenosine antagonists such as caffeine are used to enhance wakefulness (Stenberg 2007). Evidence indicates that both adenosine A 1 and A 2A receptors are involved in the regulation of sleep, though probably through different mechanisms and distinct brain areas (Stenberg 2007). Several studies have reported that sleep can be induced by systemic administration of CGS 21680 or local injections of this drug into the basal forebrain (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007).…”

“…Evidence indicates that both adenosine A 1 and A 2A receptors are involved in the regulation of sleep, though probably through different mechanisms and distinct brain areas (Stenberg 2007). Several studies have reported that sleep can be induced by systemic administration of CGS 21680 or local injections of this drug into the basal forebrain (Satoh et al 1998;Porkka-Heiskanen et al 2000;Scammell et al 2001;Hong et al 2005;Stenberg 2007). Knockout of adenosine A 2A receptors in mice resulted in a loss of sensitivity to the sedative effects of adenosine A 2A agonists, and in these studies, it also was shown that an adenosine A 2A agonist could induce sleep in wild-type mice (Satoh et al 1998).…”