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CAV1.2 calcium channel is involved in the circadian regulation of sleep
Abstracts / Sleep Medicine 14S (2013) e165–e238
good response to dopaminergic treatment and the diagnosis of idiopathic PD was established. Conclusion: We report this case because the co-occurrence of NC and PD is very rare according to the literature. Acknowledgement: IGA MZ ÈR: NT 13238–4/2012. http://dx.doi.org/10.1016/j.sleep.2013.11.408
CAV1.2 calcium channel is involved in the circadian regulation of sleep D. Kumar, N. Dedic, C. Flachskamm, J. Deussing, M. Kimura Max Planck Institute of Psychiatry, Germany
Introduction: Two L-type Ca2+ channels (Cav1.2 & Cav1.3) are expressed in the mouse brain with Cav1.2 contributing to a major proportion (85%). The expression of L-type Ca2+ channels is greatly densed in the suprachiasmatic nuclei, a neuronal area capable of functioning as autonomous clock and as a generator of circadian rhythms. Although one of the most important aspects regarding the circadian rhythm is the sleep–wake cycle, yet the role of Cav1.2 in the sleep–wake cycle is unclear. Therefore, we investigated whether depletion of Cav1.2 in a transgenic mouse line Cav1.2 (+/ ) would alter spontaneous sleep–wake activities. Materials and methods: Sleep–wake patterns were monitored by means of EEG and EMG recordings in Cav1.2 (+/ ) mice and their wild-type littermates under baseline and sleep deprivation conditions (6 h by gentle handling). Results: Under basal condition, Cav1.2 (+/ ) mice showed increased sleep onset latency but subsequent hypersomnolence as compared to wild-type. The hypersomnolence observed in these mice was characterized by higher slow wave activity. Moreover, these heterozygous mice also exhibited drastically shorter wake episodes in the dark period, due to an increased number of NREM sleep episodes. Analysis of sleep architecture further revealed that these mice showed frequent transitions from wake to NREM sleep and vice versa. After sleep deprivation, the sleep onset latency decreased drastically and the trend for higher NREM sleep was observed in Cav1.2 (+/ ) mice. Conclusion: Our results demonstrate that depletion of Cav1.2 significantly impacts circadian sleep regulation indicated by increased NREM sleep and decreased time spent in wake in the dark period. However, homeostatic regulation of sleep was unaltered. It has been reported that L-type Ca2+ channels are involved in wake-promoting effects of hypocretin1. Therefore, decreased wakefulness in Cav1.2 (+/ ) mice suggests that a depletion of Cav1.2 might attenuate the hypocretin 1 mediated excitation of wake-related neurons. The alpha-1 subunit of L-type Ca2+ channels (Cav1.2) is encoded by the CACNA1C gene. Genome-wide association studies (GWAS) have suggested that polymorphisms in the CACNA1C gene are associated with sleep disorders, e.g., insomnia and narcolepsy. Increased sleep onset latency and fragmented sleep architecture displayed by Cav1.2 (+/ ) mice might be signs of symptomatic sleep disorders but further studies are needed to elucidate this. Nevertheless, several GWAS studies have significantly associated the CACNA1C gene with psychiatric disorders. http://dx.doi.org/10.1016/j.sleep.2013.11.409
Do fathers suffer from postpartum fatigue? The roles of sleep quality and stress T. Kushnir 1, S. Israeli-Tedgi 2, J. Urkin 3 1 Ben-Gurion University of the Negev, Faculty of Health Sciences, Israel 2 Ben-Gurion University of the Negev, Faculty of Health Sciences, Public Health Israel 3 Ben-Gurion University of the Negev, Faculty of Health Sciences, Medical Education, Israel
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Introduction: Background: Childbirth and the responsibilities of parenting require a great deal of energy. Sleep disturbances that are common in the postpartum period, are important correlates of fatigue and could affect energy levels. Postpartum fatigue (PPF) is the most common unpleasant symptom following childbirth. It is an overwhelming sense of energy loss, exhaustion and decreased capacity for physical and mental work following childbirth. There have been no direct studies of PPF and its correlates among fathers. Aims: To compare PPF levels of fathers and wives in the post delivery period; to assess the contribution of sleep quality and stress to fathers’ PPF. Materials and methods: Participants were 50 married couples (n = 100), ages 20–40, four to six weeks post delivery. They were attending routine pediatric appointments in community clinics. We excluded women with postnatal depression (based on Edinburgh Postnatal Depression Scale). A self reporting questionnaire assessed: postpartum fatigue (FCS), sleep quality (PSQI), stress (PS) and postnatal depression (EPDS). Results: PPF levels of fathers and wives were highly correlated (r = 0.644, p < .001). There were no significant differences in PPF between fathers and wives. Among fathers sleep quality was strongly correlated with stress (r = 0.690, p < .001) and PPF (r = 0.633, p < 0.01). Multicollinearity was not found. In a multiple regression analysis with sleep quality and stress as independent predictors of PPF, the effect of sleep quality on PPF was greatly reduced (r = 0.28, p < .05). A Sobel test of the significance of this reduction confirmed that stress mediated the association between sleep quality and PPF. Thus the effect of sleep quality on fatigue was indirect. Conclusion: In this preliminary investigation with a small sample, fathers and their wives in the post delivery period had similar levels of PPF. It is well known that most mothers in the post-partum period suffer from PPF. Our results indicate that this phenomenon may be common among fathers too. Thus PPF may adversely affect both mothers’ and fathers’ quality of life. Our results also suggest that among the fathers sleep issues probably raised stress levels which in turn increased PPT levels. This possibility requires further systematic confirmation. Further systematic studies are needed to uncover the extent and correlates of PPF and the interconnections between the factors implicated in this phenomenon among fathers. Acknowledgement: We acknowledge the help of Dr. Nir Madjar who greatly contributed to the statistical analysis. http://dx.doi.org/10.1016/j.sleep.2013.11.410
Period lengths of temperature and melatonin circadian rhythms in delayed sleep phase disorder G. Micic 1, L. Lack 1, N. Lovato 1, H. Burgess 2, S. Ferguson 3 1 Flinders University of South Australia, School of Psychology, Australia 2 Rush University Medical Center, Circadian Rhythms Research Laboratory, Australia 3 Central Queensland University, Appleton Institute, Australia
Introduction: Delayed Sleep Phase Disorder (DSPD) is characterized as an abnormally delayed sleep period. The currently assumed aetiology is simply a phase-delay in individuals’ biological body clocks. However, DSPD cases treated to produce a corrective phase advance are very prone to relapse. It has been suggested that this may be due to an abnormally long period length (time taken to complete one cycle of the rhythm). Circadian period lengths of endogenous core body temperature and salivary melatonin were measured to investigate this premise. Materials and methods: Following rigorous screening procedures, nine healthy controls and nine persons with DSPD were selected for a 80-h protocol consisting of an ultradian modified constant rou-
good response to dopaminergic treatment and the diagnosis of idiopathic PD was established. Conclusion: We report this case because the co-occurrence of NC and PD is very rare according to the literature. Acknowledgement: IGA MZ ÈR: NT 13238–4/2012. http://dx.doi.org/10.1016/j.sleep.2013.11.408
CAV1.2 calcium channel is involved in the circadian regulation of sleep D. Kumar, N. Dedic, C. Flachskamm, J. Deussing, M. Kimura Max Planck Institute of Psychiatry, Germany
Introduction: Two L-type Ca2+ channels (Cav1.2 & Cav1.3) are expressed in the mouse brain with Cav1.2 contributing to a major proportion (85%). The expression of L-type Ca2+ channels is greatly densed in the suprachiasmatic nuclei, a neuronal area capable of functioning as autonomous clock and as a generator of circadian rhythms. Although one of the most important aspects regarding the circadian rhythm is the sleep–wake cycle, yet the role of Cav1.2 in the sleep–wake cycle is unclear. Therefore, we investigated whether depletion of Cav1.2 in a transgenic mouse line Cav1.2 (+/ ) would alter spontaneous sleep–wake activities. Materials and methods: Sleep–wake patterns were monitored by means of EEG and EMG recordings in Cav1.2 (+/ ) mice and their wild-type littermates under baseline and sleep deprivation conditions (6 h by gentle handling). Results: Under basal condition, Cav1.2 (+/ ) mice showed increased sleep onset latency but subsequent hypersomnolence as compared to wild-type. The hypersomnolence observed in these mice was characterized by higher slow wave activity. Moreover, these heterozygous mice also exhibited drastically shorter wake episodes in the dark period, due to an increased number of NREM sleep episodes. Analysis of sleep architecture further revealed that these mice showed frequent transitions from wake to NREM sleep and vice versa. After sleep deprivation, the sleep onset latency decreased drastically and the trend for higher NREM sleep was observed in Cav1.2 (+/ ) mice. Conclusion: Our results demonstrate that depletion of Cav1.2 significantly impacts circadian sleep regulation indicated by increased NREM sleep and decreased time spent in wake in the dark period. However, homeostatic regulation of sleep was unaltered. It has been reported that L-type Ca2+ channels are involved in wake-promoting effects of hypocretin1. Therefore, decreased wakefulness in Cav1.2 (+/ ) mice suggests that a depletion of Cav1.2 might attenuate the hypocretin 1 mediated excitation of wake-related neurons. The alpha-1 subunit of L-type Ca2+ channels (Cav1.2) is encoded by the CACNA1C gene. Genome-wide association studies (GWAS) have suggested that polymorphisms in the CACNA1C gene are associated with sleep disorders, e.g., insomnia and narcolepsy. Increased sleep onset latency and fragmented sleep architecture displayed by Cav1.2 (+/ ) mice might be signs of symptomatic sleep disorders but further studies are needed to elucidate this. Nevertheless, several GWAS studies have significantly associated the CACNA1C gene with psychiatric disorders. http://dx.doi.org/10.1016/j.sleep.2013.11.409
Do fathers suffer from postpartum fatigue? The roles of sleep quality and stress T. Kushnir 1, S. Israeli-Tedgi 2, J. Urkin 3 1 Ben-Gurion University of the Negev, Faculty of Health Sciences, Israel 2 Ben-Gurion University of the Negev, Faculty of Health Sciences, Public Health Israel 3 Ben-Gurion University of the Negev, Faculty of Health Sciences, Medical Education, Israel
e175
Introduction: Background: Childbirth and the responsibilities of parenting require a great deal of energy. Sleep disturbances that are common in the postpartum period, are important correlates of fatigue and could affect energy levels. Postpartum fatigue (PPF) is the most common unpleasant symptom following childbirth. It is an overwhelming sense of energy loss, exhaustion and decreased capacity for physical and mental work following childbirth. There have been no direct studies of PPF and its correlates among fathers. Aims: To compare PPF levels of fathers and wives in the post delivery period; to assess the contribution of sleep quality and stress to fathers’ PPF. Materials and methods: Participants were 50 married couples (n = 100), ages 20–40, four to six weeks post delivery. They were attending routine pediatric appointments in community clinics. We excluded women with postnatal depression (based on Edinburgh Postnatal Depression Scale). A self reporting questionnaire assessed: postpartum fatigue (FCS), sleep quality (PSQI), stress (PS) and postnatal depression (EPDS). Results: PPF levels of fathers and wives were highly correlated (r = 0.644, p < .001). There were no significant differences in PPF between fathers and wives. Among fathers sleep quality was strongly correlated with stress (r = 0.690, p < .001) and PPF (r = 0.633, p < 0.01). Multicollinearity was not found. In a multiple regression analysis with sleep quality and stress as independent predictors of PPF, the effect of sleep quality on PPF was greatly reduced (r = 0.28, p < .05). A Sobel test of the significance of this reduction confirmed that stress mediated the association between sleep quality and PPF. Thus the effect of sleep quality on fatigue was indirect. Conclusion: In this preliminary investigation with a small sample, fathers and their wives in the post delivery period had similar levels of PPF. It is well known that most mothers in the post-partum period suffer from PPF. Our results indicate that this phenomenon may be common among fathers too. Thus PPF may adversely affect both mothers’ and fathers’ quality of life. Our results also suggest that among the fathers sleep issues probably raised stress levels which in turn increased PPT levels. This possibility requires further systematic confirmation. Further systematic studies are needed to uncover the extent and correlates of PPF and the interconnections between the factors implicated in this phenomenon among fathers. Acknowledgement: We acknowledge the help of Dr. Nir Madjar who greatly contributed to the statistical analysis. http://dx.doi.org/10.1016/j.sleep.2013.11.410
Period lengths of temperature and melatonin circadian rhythms in delayed sleep phase disorder G. Micic 1, L. Lack 1, N. Lovato 1, H. Burgess 2, S. Ferguson 3 1 Flinders University of South Australia, School of Psychology, Australia 2 Rush University Medical Center, Circadian Rhythms Research Laboratory, Australia 3 Central Queensland University, Appleton Institute, Australia
Introduction: Delayed Sleep Phase Disorder (DSPD) is characterized as an abnormally delayed sleep period. The currently assumed aetiology is simply a phase-delay in individuals’ biological body clocks. However, DSPD cases treated to produce a corrective phase advance are very prone to relapse. It has been suggested that this may be due to an abnormally long period length (time taken to complete one cycle of the rhythm). Circadian period lengths of endogenous core body temperature and salivary melatonin were measured to investigate this premise. Materials and methods: Following rigorous screening procedures, nine healthy controls and nine persons with DSPD were selected for a 80-h protocol consisting of an ultradian modified constant rou-