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Sleep/wake Cycle (wake + cycle)
Selected AbstractsInterleukin-1, Induces Cyclooxygenase-2 and Prostaglandin E2 Synthesis in Human Neuroblastoma CellsJOURNAL OF NEUROCHEMISTRY, Issue 5 2000Involvement of p38 Mitogen-Activated Protein Kinase, Nuclear Factor- Abstract: Prostaglandins (PGs), which are generated by the enzymatic activity of cyclooxygenase (COX)-1 and -2, modulate several functions in the CNS such as the generation of fever, the sleep/wake cycle, and the perception of pain. Moreover, the neuronal induction of COX-2 has been linked to neuroinflammatory aspects of Alzheimer's disease (AD). The regulation of COX expression in neuronal cells is only partly understood and has been mainly linked to synaptic activity. In pathophysiological situations, however, cytokines may be potent stimulators of neuronal COX expression. Here we show that interleukin (IL)-1, induces COX-2 mRNA and protein synthesis and the release of PGE2 in the human neuroblastoma cell line SK-N-SH. We further demonstrate that both a free radical scavenger and an inhibitor of p38 mitogen-activated protein kinase (MAPK) reduce IL-1,-induced synthesis of COX-2. IL-1, induces p38 MAPK phosphorylation and activation of the nuclear factor-,B independently from each other. Our data suggest that IL-1,-induced COX-2 expression in SK-N-SH cells is regulated by different mechanisms, presumably involving mRNA transcription and mRNA stability. The ability of p38 MAPK to augment COX-2 expression in human neuroblastoma cells, as shown here, suggests that p38 MAPK may be involved in neuronal expression of COX-2 in AD. [source] Prenatal protein malnourished rats show changes in sleep/wake behavior as adultsJOURNAL OF SLEEP RESEARCH, Issue 1 2000Subimal Datta SUMMARY Prenatal protein malnutrition significantly elevates brain levels of serotonin in rats, and these levels remain elevated throughout their lives. This biogenic amine is involved in the regulation of many physiological functions, including the normal sleep/wake cycle. The present study examined the effects of prenatal protein malnutrition on the sleep/wake cycle of freely moving adult rats. Six prenatally protein malnourished (6% casein) and 10 well-nourished (25% casein) male rats (90,120-day-old) were chronically implanted with a standard set of electrodes (to record cortical electroencephalogram, neck muscle electromyogram, electrooculogram, and hippocampal theta wave) to objectively measure states of sleep and wakefulness. Six-hour polygraphic recordings were made between 10.00 and 16.00 h; a time when the rats normally sleep. Prenatally malnourished rats spent 20% more time in slow wave sleep (SWS) compared to the well-nourished rats. The total percentage of time spent in rapid eye movement (REM) sleep was 61% less in prenatally malnourished rats compared to well-nourished control rats. These findings demonstrate the adverse consequences of prenatal protein malnutrition on the quality and quantity of adult sleep in rats. These sleep changes are potentially detrimental to normal social behavior and cognitive functions. Prenatally malnourished rats are an excellent animal model to study the role of endogenous serotonin in the regulation of the normal sleep/wake cycle. [source] High-throughput behavioral phenotyping in the expanded panel of BXD recombinant inbred strainsGENES, BRAIN AND BEHAVIOR, Issue 2 2010V. M. Philip Genetic reference populations, particularly the BXD recombinant inbred (BXD RI) strains derived from C57BL/6J and DBA/2J mice, are a valuable resource for the discovery of the bio-molecular substrates and genetic drivers responsible for trait variation and covariation. This approach can be profitably applied in the analysis of susceptibility and mechanisms of drug and alcohol use disorders for which many predisposing behaviors may predict the occurrence and manifestation of increased preference for these substances. Many of these traits are modeled by common mouse behavioral assays, facilitating the detection of patterns and sources of genetic coregulation of predisposing phenotypes and substance consumption. Members of the Tennessee Mouse Genome Consortium (TMGC) have obtained phenotype data from over 250 measures related to multiple behavioral assays across several batteries: response to, and withdrawal from cocaine, 3,4-methylenedioxymethamphetamine; "ecstasy" (MDMA), morphine and alcohol; novelty seeking; behavioral despair and related neurological phenomena; pain sensitivity; stress sensitivity; anxiety; hyperactivity and sleep/wake cycles. All traits have been measured in both sexes in approximately 70 strains of the recently expanded panel of BXD RI strains. Sex differences and heritability estimates were obtained for each trait, and a comparison of early (N = 32) and recent (N = 37) BXD RI lines was performed. Primary data are publicly available for heritability, sex difference and genetic analyses using the MouseTrack database, and are also available in GeneNetwork.org for quantitative trait locus (QTL) detection and genetic analysis of gene expression. Together with the results of related studies, these data form a public resource for integrative systems genetic analysis of neurobehavioral traits. [source] Fetal Heart Rate Patterns and Sudden Infant Death SyndromeJOURNAL OF OBSTETRIC, GYNECOLOGIC & NEONATAL NURSING, Issue 1 2006Cydney A. Menihan Objective:, To determine differences in electronic fetal monitoring patterns between infants who died of sudden infant death syndrome and controls. Design:, Case-control study (N= 127). Setting:, A tertiary-level women's hospital in Providence, Rhode Island. Participants:, Infants born between 1990 and 1998 who subsequently died of sudden infant death syndrome and controls. Demographic and clinical data included medical maternal charts and fetal monitoring records. Results:, Compared with controls (n= 98), the mothers whose infants subsequently died of sudden infant death syndrome (n= 29) had lower birthweight babies (sudden infant death syndrome 2,840 vs. controls 3,385 g; p < .01), were younger (22 vs. 28 years; p < .01), were more likely to receive Medicaid health insurance (odds ratio 4.6; confidence interval 1.9-11.2), were more likely to be unmarried (odds ratio 5.2; confidence interval 2.1-12.8), had less intention to breastfeed (26% vs. 57%), and were more likely to smoke (odds ratio 4.6; confidence interval 9-11.2). Main outcome measures:, There were no statistical differences in fetal heart rate variability or sleep/wake cycles detected between groups. Conclusion:, Statistical differences were found in demographic characteristics between sudden infant death syndrome mother-infant couples and their controls. However, no differences were detected in the intrapartum electronic fetal monitoring records, specifically in variability and sleep/wake cycles. JOGNN,35, 116,122; 2006. DOI: 10.1111/J.1552-6909.2006.00013.x [source] | |||||||||||||