title: Metabolic response of the cerebral cortex following gentle sleep deprivation and modafinil administration.
abstract: OBJECTIVE
  The main energy reserve of the brain is glycogen, which is almost exclusively localized in astrocytes. We previously reported that cerebral expression of certain genes related to glycogen metabolism changed following instrumental sleep deprivation in mice. Here, we extended our investigations to another set of genes related to glycogen and glucose metabolism. We also compared the effect of instrumentally and pharmacologically induced prolonged wakefulness, followed (or not) by 3 hours of sleep recovery, on the expression of genes related to brain energy metabolism.
  
  
  METHODS
  Sleep deprivation for 6-7 hours.
  
  
  METHODS
  Animal sleep research laboratory.
  
  
  METHODS
  Adults OF1 mice.
  
  
  METHODS
  Wakefulness was maintained by "gentle sleep deprivation" method (GSD) or by administration of the wakefulness-promoting drug modafinil (MOD) (200 mg/kg i.p.).
  
  
  RESULTS
  Levels of mRNAs encoding proteins related to energy metabolism were measured by quantitative real-time PCR in the cerebral cortex. The mRNAs encoding protein targeting to glycogen (PTG) and the glial glucose transporter were significantly increased following both procedures used to prolong wakefulness. Glycogenin mRNA levels were increased only after GSD, while neuronal glucose transporter mRNA only after MOD. These effects were reversed after sleep recovery. A significant enhancement of glycogen synthase activity without any changes in glycogen levels was observed in both conditions.
  
  
  CONCLUSIONS
  These results indicate the existence of a metabolic adaptation of astrocytes aimed at maintaining brain energy homeostasis during the sleep-wake cycle.
authors.affiliation: Laboratory of Neuroenergetic and Cellular Dynamics, Brain Mind Institute, Life Science Faculty, EPFL, Lausanne, Switzerland. jean-marie.petit@epfl.ch
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Petit
authors.forename: Irene
authors.initials: I
authors.lastname: Tobler
authors.forename: Caroline
authors.initials: C
authors.lastname: Kopp
authors.forename: Florence
authors.initials: F
authors.lastname: Morgenthaler
authors.forename: Alexander A
authors.initials: AA
authors.lastname: Borbély
authors.forename: Pierre J
authors.initials: PJ
authors.lastname: Magistretti
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds; D000697:Central Nervous System Stimulants; D002540:Cerebral Cortex / Q000378:metabolism*; D004195:Disease Models, Animal; D004734:Energy Metabolism; D015870:Gene Expression; D051246:Glucose Transport Proteins, Facilitative / Q000378:metabolism; D005964:Glucosyltransferases / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D008297:Male; D051379:Mice; D000077408:Modafinil; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012892:Sleep Deprivation / Q000139:chemically induced / Q000378:metabolism*; D014851:Wakefulness / Q000502:physiology
chemical_list: D001559:Benzhydryl Compounds; D000697:Central Nervous System Stimulants; D051246:Glucose Transport Proteins, Facilitative; D006023:Glycoproteins; D012333:RNA, Messenger; C051887:glycogenin; D006003:Glycogen; D005964:Glucosyltransferases; D006006:Glycogen Synthase; D000077408:Modafinil