title: Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation.
abstract: BACKGROUND
  Selective rapid eye movement sleep (REMS) deprivation using the platform-on-water ("flower pot") method causes sleep rebound with increased REMS, decreased REMS latency, and activation of the melanin-concentrating hormone (MCH) expressing neurons in the hypothalamus. MCH is implicated in the pathomechanism of depression regarding its influence on mood, feeding behavior, and REMS.
  
  
  OBJECTIVE
  We investigated the effects of the most selective serotonin reuptake inhibitor escitalopram on sleep rebound following REMS deprivation and, in parallel, on the activation of MCH-containing neurons.
  
  
  METHODS
  Escitalopram or vehicle (10 mg/kg, intraperitoneally) was administered to REMS-deprived (72 h) or home cage male Wistar rats. During the 3-h-long "rebound sleep", electroencephalography was recorded, followed by an MCH/Fos double immunohistochemistry.
  
  
  RESULTS
  During REMS rebound, the time spent in REMS and the number of MCH/Fos double-labeled neurons in the lateral hypothalamus increased markedly, and REMS latency showed a significant decrease. All these effects of REMS deprivation were significantly attenuated by escitalopram treatment. Besides the REMS-suppressing effects, escitalopram caused an increase in amount of and decrease in latency of slow wave sleep during the rebound.
  
  
  CONCLUSIONS
  These results show that despite the high REMS pressure caused by REMS deprivation procedure, escitalopram has the ability to suppress REMS rebound, as well as to diminish the activation of MCH-containing neurons, in parallel. Escitalopram caused a shift from REMS to slow wave sleep during the rebound. Furthermore, these data point to the potential connection between the serotonergic system and MCH in sleep regulation, which can be relevant in depression and in other mood disorders.
authors.affiliation: Department of Pharmacodynamics, Semmelweis University, 1089 Nagyvárad tér 4., Budapest, Hungary.
authors.forename: Zita
authors.initials: Z
authors.lastname: Kátai
authors.forename: Csaba
authors.initials: C
authors.lastname: Adori
authors.forename: Tamás
authors.initials: T
authors.lastname: Kitka
authors.forename: Szilvia
authors.initials: S
authors.lastname: Vas
authors.forename: Lajos
authors.initials: L
authors.lastname: Kalmár
authors.forename: Diána
authors.initials: D
authors.lastname: Kostyalik
authors.forename: László
authors.initials: L
authors.lastname: Tóthfalusi
authors.forename: Miklós
authors.initials: M
authors.lastname: Palkovits
authors.forename: György
authors.initials: G
authors.lastname: Bagdy
mesh_terms: D000818:Animals; D015283:Citalopram / Q000008:administration & dosage / Q000494:pharmacology*; D004569:Electroencephalography; D007028:Hypothalamic Hormones / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008543:Melanins / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D010907:Pituitary Hormones / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D017367:Selective Serotonin Reuptake Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D012892:Sleep Deprivation / Q000378:metabolism / Q000503:physiopathology; D012895:Sleep, REM / Q000187:drug effects*; D013997:Time Factors
chemical_list: D015283:Citalopram; D007028:Hypothalamic Hormones; D008543:Melanins; D010907:Pituitary Hormones; D017367:Selective Serotonin Reuptake Inhibitors; C019463:melanin-concentrating hormone