SLEEP 2011 Abstract Supplement

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A. Basic Science II. Cell and Molecular Biology and Genetics 0036 NADPH OXIDASE 2 ACTIVATION IN MOUSE BRAIN DURING INTERMITTENT HYPOXIA PROMOTES EXCESSIVE MITOCHONDRIAL ROS PRODUCTION AND DYSFUNCTION Zhang S, Qiao Z, Gozal D, Wang Y University of Chicago, Chicago, IL, USA Introduction: We recently showed that intermittent hypoxia during sleep (IH)-induced neuronal oxidative stress and neurocognitive deficits in mice were closely related to increased reactive oxygen species (ROS) content and impaired respiratory function in cortical and hippocampal mitochondria. On the other hand, these IH-induced pathological changes were shown to be abolished or attenuated in mice in which NADPH oxidase was genetically inactivated or pharmacologically inhibited. The interaction between the NADPH oxidase pathway and pathways underlying excessive mitochondrial ROS production is however unclear. Methods: C57BL/6 and gp91phox-/- mice were exposed to IH (alternating 5.7% and 21% O2 every 90 seconds 12 hours/day for 2 months). Cortical mitochondria were isolated for assessment of ROS content, membrane potential, and electron transport chain complex activities. Results: IH elicited significant increases in ROS content in cortical mitochondria isolated from C57BL/6 mice, especially when respiration was supported by a complex II substrate. Addition of ADP reduced mitochondrial ROS content in both control and IH-treated animals and completely abolished the difference between the two groups. Cortical mitochondria from IH-treated C57BL/6 mice were also characterized by decreased complex I activity and reduced inner mitochondrial membrane potential. In contrast, IH-induced increases in cortical mitochondrial ROS content were significantly attenuated in gp91phox-/- mice lacking NADPH oxidase 2 activities due to disruption of the gene encoding the catalytic subunit of the enzyme. Furthermore, IH-induced impairment of complex I activity and inner mitochondrial membrane potential were abrogated in gp91phox-/- mice. Conclusion: Our findings suggest the presence of a cross-talk between the NADPH oxidase 2 and mitochondrial ROS production pathways, in which the former triggers the latter to generate excessive amounts of ROS. Excess ROS production in turn, leads to mitochondrial oxidative stress and dysfunction in cortical mitochondria of mice exposed to IH, promoting apoptosis and cellular dysfunction. Support (If Any): Supported by NIH grants HL-074369 and HL- 086662. 0037 CORTICAL WHITE MATTER IS VULNERABLE TO INTERMITTENT HYPOXIA IN NKX6.2 NULL MICE Cai J 1 , Tuong C 2 , Gozal D 3 1 Pediatrics/KCH Res. Inst., Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY, USA, 2 Pediatrics/KCH Res. Inst., University of Louisville School of Medicine, Louisville, KY, USA, 3 Pediatrics, University of Chicago, Chicago, IL, USA Introduction: Recent studies demonstrate that white matter is extensively affected in brains of obstructive sleep apnea (OSA) patients. We hypothesize that developmental myelin defect or breakdown underlies the vulnerability of brain white matter to sleep apnea-associated IH. To test this hypothesis, we examined the molecules relevant to myelin architecture and oligodendrocytes in the mouse model of sleep apnea-associated intermittent hypoxia (IH) using Nkx6.2-null mutant mice with characteristics of mild abnormal paranodes and slight hypomyelination. Methods: 12-week C57BL wild-type and Nkx6.2-null mice were exposed to intermittent hypoxia (IH, 8% / 20.9% O2 /120s each cycle/12hrs) or intermittent air (IA) during the light phase. After two-week IA or IH exposure, prefrontal cortex, cortex, CA1 region and cerebellum were dissected and collected. Myelin-related proteins, structural molecules of paranode/node of Ranvier, and adult oligodendrocyte progenitor cells (aOPCs) were examined in different brain regions between IA- and IHtreated young adult wild-type or Nkx6.2 null mice. Results: The expressions of myelin-relevant molecules including MBP and CNPase were significant decreased in cortex, especially in prefrontal area, in Nkx6.2-null brains after 2-week IH exposure. The NG2+/ pdgfrα+ aOPCs proliferated in response to IH insult. However, no obvious phenotype of myelin was observed in IH-insulted wild-type brains. Conclusion: The white matter in region of cortex with myelin deficiency is vulnerable and sensitive to short-term IH insult, which may further lead to neurological disorders. Intact and compact myelin laminate may protect axons against short-term IH insult. Support (If Any): Sleep Research Society Foundation/J. Christian Gillin M.D. Research Grant (J.C.), University of Louisville SOM Basic Grant (J.C.), and NIH HL-086662 (D.G.) 0038 EFFECTS OF STRESSOR CONTROLLABILITY ON NEURAL PLASTICITY ASSOCIATED MRNA LEVELS IN MOUSE AMYGDALA AND MEDIAL PREFRONTAL CORTEX (MPFC) Machida M, Lonart G, Yang L, Sanford LD Pathology & Anatomy, Eastern Virginia Medical School, Norfolk, VA, USA Introduction: Controllable and uncontrollable stress, modeled by escapable and inescapable shock (ES and IS), produce different alterations in post-stress rapid eye movement sleep (REM; ES increases whereas IS decreases). Conditioned reminders of ES and IS also produce increases and decreases in REM similar to those seen with the original stressors. The mPFC assesses stressor controllability and interacts with the amygdala which regulates post-stress sleep and conditioned changes in sleep. We examined the expression of genes linked to neural plasticity in the mPFC and amygdala after training with ES and IS. Methods: Male BALB/cJ mice were trained in a shuttlebox using a yoked design such that pairs of ES and IS mice received identical amounts of shock (20 shocks: 0.5 mA, 5.0 sec maximum duration, 1.0 min intervals), but only ES mice could terminate shock. Control animals (NS) were treated identically, but did not receive shock. Immediately or 2 hour after training, animals were sacrificed, total RNA was isolated, then reverse transcription and real-time quantitative PCR (RT 2 qPCR) was performed to assess mRNA levels of RIM1, BDNF, NGF-β, TNFα, FGF-2, Arc, c-Fos, zif268, GRPR, spinophilin and GluR1 genes in the amygdala, mPFC and somatosensory cortex, a control region. Corticosterone was examined at each time point as an index of the stress response. Results: ES produced a significant up-regulation of BDNF mRNA levels at 2 hour post-training in both regions. ES also significantly elevated zif268 and GluR1 mRNA levels in mPFC whereas IS significantly elevated Arc and GRPR mRNA levels in the amygdala. ES and IS did not differentially alter mRNA levels in the somatosensory cortex. Corticosterone was similarly increased by ES and IS compared to NS. Conclusion: The observed differences in zif268, GluR1, Arc, and GRPR mRNA levels after ES and IS may be due to differential expression of neuronal plasticity related genes in the mPFC and amygdala. Activation of divergent cellular pathways may underlie differences in behavior and sleep produced by controllable and uncontrollable stress and their associated memories. Support (If Any): Supported by NIH research grants MH61716 and MH64827. SLEEP, Volume 34, Abstract Supplement, 2011 A16
A. Basic Science II. Cell and Molecular Biology and Genetics 0039 IN VIVO MICRORNA-138 INHIBITION SUPRESSES SLEEP AND DELTA POWER DURING THE LIGHT PHASE Davis CJ 1,2,3 , Clinton JM 1,2,3 , Bohnet SG 1,2,3 , Krueger JM 1,2,3 1 WWAMI Medical Education Program, Washington State University- Spokane, Spokane, WA, USA, 2 Sleep and Performance Research Center, Washington State University-Spokane, Spokane, WA, USA, 3 Program in Neuroscience, Washington State University-Spokane, Spokane, WA, USA AcPb mRNA in the rat SSctx was significantly increased after SD compared with the control group and during the daily cycle was highest (2 fold) 4h after dark onset and lowest values were observed 8h after light onset (p
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