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1 Neurosciences program, Stanford University, Stanford, CA, USA; Biological Sciences, Stanford University, Stanford, CA, USA
2 Faculte de Medecine, Centre de National de la Recherche Scientifiqu (CNRS), Lyon, France
3 Biological Sciences, Stanford University, Stanford, CA, USA
4 Biological Sciences, Stanford University, Stanford, CA, USA; Neurosciences program, Stanford University, Stanford, CA, USA
5 Department of Biology, University of Kentucky, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: Ilana.Hairston{at}stanford.edu.
The sleeping brain differs from the waking brain in its electrophysiological and molecular properties, including the expression of growth factors and immediate early genes (IEG). Sleep architecture and homeostatic regulation of sleep in neonates is distinct from that of adults. Hence, the present study addressed the question whether the unique homeostatic response to sleep deprivation in neonates is reflected in mRNA expression of the IEG cFos, brain-derived nerve growth factor (BDNF), and basic fibroblast growth factor (FGF2) in the cortex. As sleep deprivation is stressful to developing rats, we also investigated whether the increased levels of corticosterone would affect the expression of growth factors in the hippocampus, known to be sensitive to glucocorticoid levels. At postnatal days 16, 20, and 24 rats were subjected to either sleep deprivation, maternal separation without sleep deprivation, sleep deprivation with two hours recovery sleep, or no intervention. mRNA expression was quantified in the cortex and hippocampus. cFos was increased after sleep deprivation, and was similar to control level after two hours recovery sleep irrespective of age or brain region. BDNF was increased by sleep deprivation in the cortex at P20 and P24, and only at P24 in the hippocampus. FGF2 increased during recovery sleep at all ages in both brain regions. We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, while the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation.
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