SLEEP 2011 Abstract Supplement

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A. Basic Science V. Physiology Results: The results showed that the sleep architecture changed in general in both genders. These alterations occurred in the light and dark period, and began on D1 and persisted until the end of study. OA rats regardless the gender showed a fragmented sleep pattern with reduced sleep efficiency, slow wave sleep, and paradoxical sleep, as well as with fewer paradoxical sleep bouts. However, the males showed lower sleep efficiency and slow wave sleep compared to females in the dark period. Additionally, OA affected the hormonal levels in the male rats, as testosterone levels were reduced compared with the control and sham groups. In female, progesterone and estradiol remained unchanged during the study. Conclusion: Thus, our results suggest that the chronic model of OA influenced sleep pattern on both genders, however, males appear to be more affected. Support (If Any): Research supported by AFIP and FAPESP (CEPID #98/14303-3 to S.T. and #07/56620-6 to A.S.). Sergio Tufik and Monica Andersen are recipients of fellowships from CNPq. 0122 COADJUVANT-INDUCED ARTHRITIS ALTERS THE SLEEP ARCHITECTURE AND IMMUNE PARAMETERS OF PARTIALLY OR TOTALLY HYPOPHYSECTOMIZED LEWIS RATS Esqueda-León E 1 , Rojas Zamorano J 1 , Gomez-Gonzalez B 1 , Dominguez-Salazar E 1 , Tarrago-Castellanos M 1 , Jimenez-Anguiano A 1 , Santana-Miranda R 1 , Quintanar-Stephano A 2 , Besedovsky HO 3 , Velázquez-Moctezuma J 1 1 Biologia de la Reproduccion, Universidad Autonoma Metropolitana, Mexico, Mexico, 2 Fisiologia y Farmacologia, Universidad Autonoma de Aguascalientes Metropolitana, Aguascalientes, Mexico, 3 Immunophysiology, Marburg University, Deutschhausstrasse, Germany Introduction: Every organism requires adequate communication between the nervous, immune and endocrine systems to ensure proper functioning of the body. When such communication is disrupted, may affects the others two systems, or cause a compensatory changes to maintain the equilibrium. One disease that disrupt all three system is arthritis. Rheumatoid arthritis affects 1% of adult human population; it is a systemic autoimmune disease characterized by chronic inflammation and stiffness of several joints, enhanced pro-inflammatory cytokine levels, pain and anorexia. Clinical reports have found that many rheumathoid arthritis patients present sleep complains such as difficulty falling asleep, poor quality sleep,and sleep fragmentation, however little is known about the mechanism that induces the sleep changes observed in rheumatoid arthritis patients. Methods: In order to better describe the changes in the sleep-wake cycle architecture and to elucidate the mechanism by which rheumatoid arthritis induces sleep disruption we used an animal model of chronic joint inflammation in the Lewis rat. Fifty male Lewis rats, 300g body weight, were implanted for electroencephalographic and electromiographic recordings. Subjects were randomly assigned to one of five groups: intact animals, anterior hypophysectomy, posterior hypophysectomy, total hypophysectomy and sham-surgery controls (ten subjects each group). Fifteen days post-hypophysectomy a 24-hour polisomnographic record was carried on. Thereafter all subjects were intradermally injected with Freund’s adjuvant supplemented with Mycobacterium tuberculous at the base of the tail. Post-immunization polisomnographic recordings were carried on at days 6, 11, and 15, during the maximal immune response. At post-immunization day 16, serum, and spleen samples were obtained to characterize the immune state. Results: Differences between groups will be presented and also the values obtained in interleukines and corticosterone levels. Conclusion: The results are still being analyzed, show that the process of rheumatoid arthritis induction, had significant effects on sleep architecture, when the individual lacks some or all of the pituitary hormone action. Support (If Any): This work was supported by PROMEP program “Red de estudios sobre la integración neuro-inmuno-endocrina” and UAM-I-CA-3. 0123 EVALUATION OF POST-MENOPAUSAL BREAST CANCER SURVIVORS WITH SLEEP DISTURBANCES AND HOT FLASHES Otte JL 1 , Johnson P 2 , Carpenter JS 1 , (Cobra) C 3 , Skaar TC 3 1 Adult Health, Indiana University School of Nursing, Indianapolis, IN, USA, 2 Psychiatry, Indiana University, Indianapolis, IN, USA, 3 Medicine, Indiana University, Indianapolis, IN, USA WITHDRAWN 0124 THE SLEEP-REGULATORY ROLE OF INTERLEUKIN-1 RECEPTOR ACCESSORY PROTEIN B IN MICE Bayomy OF 1 , Zielinski MR 1 , Taishi P 1 , Smith DE 2 , Krueger JM 1 1 WWAMI Medical Education Program, Sleep and Performance Research Center, Washington State University, Spokane, WA, USA, 2 Department of Inflammation Research, Amgen, Seattle, WA, USA Introduction: Interleukin-1beta (IL1) has several functions including regulation of sleep, cerebral blood flow and inflammation. The IL1 receptor accessory protein (IL1RAcP) is required for IL1 signaling; a brain specific, alternatively spliced, form of IL1RAcP called AcPb interferes with IL1-IL1RAcP signaling. The goal of this study was to test the hypothesis that AcPb knock-out (KO) mice will sleep more in response to sleep deprivation (SD). Methods: Male IL1RAcPbKO and C57BL/6 controls were surgically implanted with EEG and EMG electrodes for sleep analysis. Spontaneous sleep and sleep responses following 6 h of SD were analyzed by established criteria. EEG power analyses of non-rapid eye movement sleep (NREMS) epochs were also performed. Results: In both strains of mice, duration of spontaneous NREMS and REMS exhibited diurnal rhythms with greater amounts of sleep observed in light periods than in dark periods (P < 0.001 for each). NREMS EEG slow wave activity (0.5-4Hz) (SWA) also exhibited a diurnal rhythm during spontaneous sleep (P < 0.001). SD significantly enhanced duration of NREMS and REMS in both strains (P < 0.001 for each). However, there were no significant differences between strains in duration of NREMS or REMS following SD. SD significantly enhanced NREMS EEG SWA during the first two post-SD hours in both strains (P = 0.002). However, NREMS EEG SWA responses to SD were not different in AcPbKO mice compared to controls. Conclusion: IL1RAcPbKO mice have similar spontaneous sleep and sleep responses to SD as C57BL/6 mice. IL1 is involved in many aspects of sleep regulation, including changes in sleep associated with pathology. Nevertheless, current results suggest that AcPb may not be involved in the IL1-IL1RAcP-sleep signaling pathway. Support (If Any): NIH NS025378, NS031453 0125 THETA ALTERATIONS AND EPILEPTIFORM ACTIVITY DURING REM SLEEP IN THE NEONATALLY-TREATED CLOMIPRAMINE RAT MODEL McDowell AL 1,2 , Feng P 1,2 , Strohl KP 1,2 1 Pulmonary Critical Care & Sleep Medicine, Case Western Reserve University, Cleveland, OH, USA, 2 Louis Stokes DVAMC, Cleveland, OH, USA Introduction: Cortical and subcortical spectral power activities vary according to pathology-specific to sleep and mood disorders (Buysse et al., SLEEP, Volume 34, Abstract Supplement, 2011 A46
A. Basic Science V. Physiology 2001). The hippocampal theta rhythm is a prominent electrophysiological marker for REM sleep (Benington et al., 1994) and has been shown to affect cortical pathways in depressed humans (Pizzagalli, et al., 2003). Furthermore, variability in spectral power also indicates epileptiform activity (see Benbadis & Rielo, 2010). Methods: Neonate Long Evans Hooded male rats were injected s.c. with CLI 20 mg/kg (n=5) or equivolume saline (n=5) twice daily for two weeks (postnatal day 8 to 21). At 5 to 6 mos. of age, rats were anesthetized and surgically implanted with recording electrodes: 5 EEG electrodes were implanted into the skull and 3 EMG electrodes were stitched into the nuchal muscle. Following recovery, animals were moved to individual sleep chambers for 3 days adaptation prior to a baseline recording (24 hours) monitored with Somnologica software. Results: The data show that CLI animals had increased REM sleep fragmentation, consistent with prior reports. There was a new finding of dramatic differences in EA, with CLI rats experiencing significantly more EA than SAL rats and a switch in theta activity at the NREM-to- REM transition. Conclusion: We conclude that EA may be playing a role in the depressive phenotype, including REM sleep fragmentation and alterations in theta rhythm. These results support a need for further examination of a comorbidity of EA, as well as sleep disturbances in patients with MDD. Support (If Any): VA Merit award, NIH training grant T32- 5THL007913-10 and Louis Stokes Cleveland VA Medical Service 0126 POST- AND PRESYNAPTIC EXCITATION OF BASAL FOREBRAIN CHOLINERGIC NEURONS BY OREXIN Ferrari LL, Mokizuki T, Yamamoto M, Scammell TE, Arrigoni E Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA Introduction: The orexin neurons play an essential role in driving arousal and maintaining wakefulness. Lack of orexin neurotransmission produces a chronic state of hypoarousal characterized by excessive sleepiness, frequent transitions between wakefulness and sleep, and episodes of cataplexy. The basal forebrain is an important component of the ascending arousal system and may be a key site through which the orexin neurons promote arousal. Here we study the effects of orexin on the cholinergic neurons of the substantia innominata (SI) using patchclamp recordings in brain slices of mice. Methods: Recordings were conducted in wild-type (WT) mice and in mice lacking the Ox1R or Ox2R orexin receptors. In these mutant mice, the orexin receptor genes are preceded by a transcriptional disruptor (TD) sequence that prevents expression of functional Ox1R and Ox2R. We identified SI cholinergic neurons using fluorescent antibodies against the p75 receptors (Cy3-p75-IgG) steretaxically injected in the later cerebroventricle. Slices were prepared one to three days after surgery. Under fluorescent microscopy, SI cholinergic neurons appeared red and were targeted for recordings. Similar to rats, Cy3-p75-IgG labeled only cholinergic neurons in the basal forebrain of mice. Results: Orexin-A (300 nM) directly excited SI cholinergic neurons and increased the glutamatergic input to these cells. Post-synaptically, orexin-A depolarized the SI cholinergic neurons by the activation of an inward current (Vh = -60 mV). In addition orexin-A increased the frequency of spontaneous excitatory postsynaptic currents (EPSCs) and this effect was blocked by the orexin receptor antagonist SB 334867 which at 10uM appears to block both Ox1 and Ox2 receptors. The effect of orexin-A on the glutamatergic input to SI cholinergic neurons was reduced in both the Ox1R and Ox2R TD mice compared to WT mice suggesting that presynaptic terminals are activated by both OxRs. Conclusion: These findings demonstrate that orexin directly excites SI cholinergic neurons and increases the excitatory input to these neurons by activation of both Ox1 and Ox2 receptors. Thus, while orexin acts through either Ox1R or Ox2R in most wake promoting neurons, the activation of cholinergic neurons in the basal forebrain occurs through both orexin receptors, emphasizing the importance of both pathways in promoting arousal and improving cognitive performance. Support (If Any): NHLBI (1P01HL095491), NINDS (1RO1NS061863), and the University of Milan, Italy 0127 THE RELATIONSHIP BETWEEN THETA OSCILLATION AND REM SLEEP DISTURBANCE INDUCED BY STRESSORS Hsiao Y, Chang F Department of Veterinary Medicine, National Taiwan University, Taipei, Taiwan Introduction: Disturbance of rapid eye movement sleep (REMS) is common in patients with anxiety disorders, and our previous results have demonstrated that REMS was suppressed by repeated combination stressors, an anxiety model in rats. In addition, we observed the appearance of high density of theta wave EEGs (4-7 Hz) when rats were exposed to stressors. Theta waves are dominant in REMS EEGs in rodents and the stress-induced enhancement of theta wave density is suppressed by anxiolytics. This study was designed to investigate whether the reduction of REMS after exposure to the stressors is subsequently due to the enhancement of theta oscillation. Methods: The combination stressors include footshocks and elevated plus maze (EPM). Male Wistar rats randomly received fifteen times of footshock stimuli, with the current of 5 amperes and the pulse duration of 0.1 second, within 10 minutes prior to the light onset. We interfered theta generation with a train of 100 Hz, 40 μA electrical stimuli to the median raphe nucleus (MR), which desynchronizes theta oscillation, during the footshocks. Sleep recordings were acquired for 24 hours. Results: Footschok-induced enhancement of theta wave density was suppressed by MR stimulations; footschoks increased theta power by 13.79 ± 3.9 arbitrary units and stimulation of MR during footschocks decreased theta power by 1.22 ± 0.9 arbitrary units. MR stimulation partially blocked footschock-induced decrease of exploration time during the open arms of EPM (Naïve group: 69.54 ± 24.0 sec; footshock group: 18.1 ± 6.9 sec; MR stimulation + footshock group: 36.16 ± 9.6 sec). However, disruption of theta power by MR stimulation did not alleviate the decrease of REMS induced by the combination stressors. Conclusion: Our results suggest that the increase of theta oscillation during stressors and stressor-induced REMS decrease may be mediated by different neuronal circuits. 0128 THE EFFECT OF TIME-OF-DAY AND LIGHT ON SLEEP PRESSURE MARKERS IN MICE Mongrain V 1,2,3 , Emmenegger Y 1 , Franken P 1 1 Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland, 2 Center for Advanced Research in Sleep Medicine, Sacre-Coeur Hospital of Montreal, Montreal, QC, Canada, 3 Psychiatry, Université de Montréal, Montreal, QC, Canada Introduction: Sleep homeostasis refers to the increase of a pressure for sleep during wakefulness and its dissipation during sleep. The dynamics of this process is studied through EEG markers measured during nonrapid eye movement sleep (delta power: 1-4Hz) and wakefulness (theta power: 6-9Hz). Data suggest that these hallmarks are modulated by circadian time and light. We thus assessed the effects of time-of-day and acute light exposure on the dynamics of sleep pressure markers in mice. Methods: Male C57BL/6J mice, implanted with EEG/EMG electrodes, were submitted to a 6h sleep deprivation (SD) by gentle handling starting at four different times of day: ZT0, ZT6, ZT12, or ZT18 (ZT0=Zeitgeber time 0: lights on). A week later, animals were submitted to the same SD but lights were turned off at the beginning of SD until the end of recording. Simulations were used to predict expected levels of delta power. Results: We observed that the rebound in delta power was higher after the ZT6 and ZT12 SD than after the ZT0 SD. When the SD was repeated A47 SLEEP, Volume 34, Abstract Supplement, 2011
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