Neurobiological Basis of Hypersomnia

Sleep Med Clin. 2017 Sep;12(3):265-277. doi: 10.1016/j.jsmc.2017.03.003. Epub 2017 Jun 7.

Abstract

Narcolepsy is the most well-characterized hypersomnia in both clinical and basic research fields. Narcolepsy is caused by degeneration of hypocretin-producing neurons in the hypothalamus. Although hypocretin receptor antagonists have been developed as sleep-inducing drugs, a high dose of suvorexant, a hypocretin receptor antagonist, inhibits gene expression of prepro-hypocretin to induce narcoleptic attack in wild-type mice. Prostaglandin D2 is the most potent endogenous sleep-promoting substance. Overproduction of prostaglandin D2 is involved in hypersomnia in patients with mastocytosis and African sleeping sickness or in mice after a pentylenetetrazole-induced seizure. Commercialized sleep-promoting supplements also may induce hypersomnia in humans.

Keywords: Adenosine; Cytokines; Gene-knockout mice; Hypocretin; Narcolepsy; Prostaglandin D2; Sleep-promoting supplement; Suvorexant.

Publication types

  • Review

MeSH terms

  • Animals
  • Disorders of Excessive Somnolence* / drug therapy
  • Disorders of Excessive Somnolence* / immunology
  • Disorders of Excessive Somnolence* / metabolism
  • Humans