Sleep and Brain Energy Levels: ATP Changes during Sleep
Markus Dworak, Robert W. McCarley, Tae Kim, Anna V. Kalinchuk, and Radhika Basheer Laboratory of Neuroscience, Department of Psychiatry, Veterans Affairs Boston Healthcare System and Harvard Medical School, West Roxbury, Massachusetts 02132
…Kay went for long periods of time without adequate sleep, in one instance, it was longer than two years because Kay was also not eating adequate amounts of food to raise ATP levels to produce the sleep inducing neurotransmitter adenosine. During her incarceration in 1994-95 she kept herself locked in her cell and slept the entire time. She specifically requested they lock her cell door. She was entrained to lock herself up and may have also contributed to her getting incarcerated again in 1997 so she could regain control of her situation despite the Judges failure to hear her side of the problem she was encountering.
The importance of sleep and suggestions about its physiological role have been better documented as a negative, by what happens without sleep, since prolonged sleep deprivation (SD) or sleep restriction adversely influences metabolic processes (Knutson, 2007), general emotional and physical health (Haack and Mullington, 2005), and neurocognitive behavior (Lim and Dinges, 2008). An often postulated, although not directly measured, function of sleep is to restore brain energy expended during active waking (Benington and Heller, 1995). Although constituting only 2% of body mass, brain oxygen and glucose utilization account for 20% of those of the whole organism (Magistretti,1999). Compared with wakefulness, indirect evidence that sleep reduces brain energy demands is a 44% reduction in the cerebral metabolic rate (CMR) of glucose (Maquet, 1995) and a 25% reduction in the CMR of O2 (Madsen et al., 1991).
This work was supported by a Department of Veterans Affairs Medical Research Service Award (R.B.), Deutsche Forschungsgemeinschaft Fellowship DW66/1-1 (M.D.), and National Institute of Mental Health Grant NIMH39683 (R.W.M.). We gratefully acknowledge Farzana Pervin Nipa for technical assistance, and Diane Ghera and Dewayne Williams for help with animal care. Correspondence should be addressed to Dr. Radhika Basheer, Laboratory of Neuroscience, Department of Psychiatry, Harvard Medical School, Research Health Scientist, Veterans Affairs Boston Healthcare, 1400 V.F.W. Parkway, West Roxbury, MA 02132.
E-mail: radhika_basheer@hms.harvard.edu.DOI:10.1523/JNEUROSCI.1423-10.2010
Copyright©2010 the authors 0270-6474/10/309007-10$15.00/0 The Journal of Neuroscience, June 30, 2010 • 30(26):9007–9016 • 9007
