Glucocorticoids influence brain glycogen levels during sleep deprivation

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2004-06, Vol.286 (6), p.R1057-R1062
• Main Authors: Gip, Phung, Hagiwara, Grace, Sapolsky, Robert M, Cao, Vinh H, Heller, H. Craig, Ruby, Norman F
• Format: Article
• Language: English
• Subjects: Adrenalectomy; Animals; Blood Glucose - metabolism; Brain Chemistry - drug effects; Energy Metabolism - drug effects; Female; Glucocorticoids - pharmacology; Glycogen - metabolism; Liver Glycogen - metabolism; Male; Rats; Rats, Long-Evans; Sleep Deprivation - metabolism
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00528.2003

2 Department of Biological Sciences, Stanford University, Stanford 94305; and 1 Stanford Genome Technology Center, Stanford University, Stanford, California 94304 Submitted 12 September 2003 ; accepted in final form 5 February 2004 We investigated whether glucocorticoids [i.e., corticosterone (Cort) in rats] released during sleep deprivation (SD) affect regional brain glycogen stores in 34-day-old Long-Evans rats. Adrenalectomized (with Cort replacement; Adx+) and intact animals were sleep deprived for 6 h beginning at lights on and then immediately killed by microwave irradiation. Brain and liver glycogen and glucose and plasma glucose levels were measured. After SD in intact animals, glycogen levels decreased in the cerebellum and hippocampus but not in the cortex or brain stem. By contrast, glycogen levels in the cortex of Adx+ rats increased by 43% ( P < 0.001) after SD, while other regions were unaffected. Also in Adx+ animals, glucose levels were decreased by an average of 28% throughout the brain after SD. Intact sleep-deprived rats had elevations of circulating Cort, blood, and liver glucose that were absent in intact control and Adx+ animals. Different responses between brain structures after SD may be due to regional variability in metabolic rate or glycogen metabolism. Our findings suggest that the elevated glucocorticoid secretion during SD causes brain glycogenolysis in response to energy demands. sleep homeostasis; corticosterone; blood glucose; liver glycogen and glucose; glycogen metabolism Address for reprint requests and other correspondence: P. Gip, Stanford Genome Technology Center, Stanford Univ., 855 California Ave., Palo Alto, CA 94304-8307 (E-mail: pgip{at}stanford.edu ).