Changes in brain glycogen after sleep deprivation vary with genotype

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2003-08, Vol.285 (2), p.413-R419
• Main Authors: Franken, Paul, Gip, Phung, Hagiwara, Grace, Ruby, Norman F, Heller, H. Craig
• Format: Article
• Language: English
• Subjects: Anesthesia; Animals; Brain - metabolism; Energy Metabolism - genetics; Food Deprivation; Genotype; Glucose - metabolism; Glycogen - metabolism; Homeostasis - genetics; Male; Mice; Mice, Inbred AKR; Mice, Inbred C57BL; Mice, Inbred DBA; Sleep Deprivation - genetics; Sleep Deprivation - metabolism
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00668.2002

Department of Biological Sciences, Stanford University, Stanford California 94305-5020 Submitted 30 October 2002 ; accepted in final form 25 April 2003 Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by 40% in the cortex of B6 mice, while glycogen significantly decreased by 20–38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis. mouse; sleep function and regulation; brain glycogen; glucose; energy homeostasis; food deprivation; halothane anesthesia Address for reprint requests and other correspondence: P. Franken, Dept. of Biological Sciences, 371 Serra Mall, Stanford Univ., Stanford, CA 94305-5020 (E-mail: pfranken{at}stanford.edu ).