Wakefulness and stress -
In this test, the mice were again allowed to freely explore the same behavioral chamber but with a novel ICR male mouse in the metal meshwork. Note that this ICR mouse was different from those used for social defeat stress.
During the habituation and social interaction test, mouse behaviors were video-recorded and automatically analyzed by the SMART video tracking software PanLab Harvard Apparatus, Holliston, MA, USA.
Social interaction to an ICR mouse in the metal meshwork was evaluated by the time spent in the interaction zone and the avoidance zone, which are the areas at one side of the behavioral chamber with the metal meshwork and the opposite side, respectively. To evaluate sniffing bouts with the length of seconds, we employed DeepLabCut, a deep learning-based algorithm which can accurately track respective body parts of a mouse during the social interaction test First, we extracted several images from the video data of respective mice and manually designate body parts to make training data.
After the model was trained by 50, iterations, we performed the inference of pertinent body parts in the video data and confirmed its accuracy by manual inspection. A sniffing bout was detected when the nose of an experimental mouse stayed within 2 cm of the metal meshwork enclosing an ICR target mouse for ms or more.
Immunohistochemistry for c-Fos was performed as previously described It has been shown that neuronal activation induces transient expression of c-Fos protein at the peak of 90 min Brains removed from the mice were post-fixed in the same fixative at 4 °C overnight. After three times wash with D-PBS containing 0.
After twice wash with D-PBS at RT, the sections were dried on APS-coated glass slides Matsunami Glass, Kishiwada, Japan and mounted using a coverslip with the ProLong Gold antifadant Thermo Fisher Scientific. Fluorescent images were taken with BZ-X Keyence, Osaka, Japan.
To analyze the number of c-Fos-expressing cells, we defined brain areas based on the Allen Mouse Brain Atlas and a mouse brain atlas by Paxinos and Franklin 29 , as previously described 19 , We analyzed the ventrolateral preoptic area VLPO , median preoptic nucleus MnPO , medial septum MS , lateral hypothalamus LH , laterodorsal tegmental nucleus LDT , dorsomedial hypothalamus DMH , and ventrolateral periaqueductal gray VLPAG.
We applied the Transfluor application module of the Metamorph software Molecular Devices Corporation, PA, USA to detect and count objects that are within the range of 9—30 μm in diameter and brighter than a threshold determined by adjacent background signals.
These objects were defined as c-Fos-expressing cells. We averaged the numbers of c-Fos-expressing cells in the same brain regions of two hemispheres in each mouse.
Linear regression and Pearson test were used to analyze correlations between the proportion of active periods and body temperature Fig.
The analyses were performed with Prism 8. P values less than 0. We included all the data for the analyses without any exclusion. Stress-induced sleep-like inactivity is involved in multiple aspects of social behaviors.
c The cumulative frequency of the proportion of the time spent in the avoidance left or interaction right zone shown in b. e Total time of social sniffing to an ICR target mouse during the social interaction test by manual counting. f A representative image of the experimental mouse with DeepLabCut-based labeling of respective body parts, enabling automatic detection of social sniffing.
g The relationship between total time of social sniffing with manual and automatic counting. h The number of sniffing bouts. i The duration of sniffing bouts left and its mean for individual mice right. j The relationship between the time spent in the interaction zone and the mean duration of sniffing bouts.
Each dot represents the values from an individual mouse. Stressed mice without sleep deprivation were analyzed as a whole or separately for stress-susceptible mice and stress-resilient mice. As a baseline, all the mice showed clear nocturnal behavior with high activity during the dark phase and low activity during the light phase Fig.
Although body temperature was increased during social defeat stress or cage transfer Fig. The proportion of active periods was significantly decreased during ZT 13—15, from one to three hours after the stress Fig.
Since one stressed mouse showed severe hypothermia unlike the other stressed mice, we first excluded this mouse from the analyses of body temperature.
The body temperature during the same period was decreased within the physiological range The body temperature was correlated to the proportion of active periods in both control and stressed mice Fig.
The effects of stress on active periods and body temperature dissipated before the end of the dark phase. The hypothermic stressed mouse excluded from the above analyses showed a gradual, but large, decrease in body temperature, which was peaked at 5 h ZT 17 after the stress Fig.
The body temperature at the peaked decrease was This severe hypothermia returned to the baseline before the social interaction test ZT 13—15 on the next day Fig. One day after the stress, we examined the effects of social defeat stress on social behaviors and exploratory activity in the social interaction test Fig.
Social defeat stress, but not cage transfer as the control, increased the time spent in the avoidance zone Fig. The stressed mice also spent less time in the interaction zone, though it was not statistically significant.
Notably, the times in the avoidance zone and the interaction zone showed high individual variability, as previously reported 3 , 4. The stressed mice that show social avoidance have been categorized as stress-susceptible mice, whereas those that do not show social avoidance as stress-resilient mice.
In this study, we considered that the time in the avoidance or interaction zone was changed, if it exceeded the mean value of control mice by standard deviation. A subset of mice 6 out of 13 mice, By contrast, neither the time in the avoidance or interaction zone showed significant change in another subset of mice 7 out of 13 mice, By definition, the distribution of the individual values was not overlapped between stress-susceptible mice and control mice or stress-resilient mice Supplementary Fig.
To quantify the level of social investigation, we manually counted the time of social sniffing to a target mouse of control and stressed mice, and found that social defeat stress significantly decreased the time of social sniffing Fig. To further examine the time and patten of social sniffing, we employed deep learning-based detection of animal behaviors by DeepLabCut Fig.
We first confirmed that the sniffing time determined by DeepLabCut was highly correlated to that manually determined in all the experimental groups Fig. Consistent with the manual detection of stress-induced decrease in the sniffing time, the stress decreased the number of sniffing bouts Fig.
We examined the intensity of social sniffing measured by the duration of each sniffing bout, which has been used to analyze the motivation for social interaction Whereas social sniffing intensity was not significantly altered Fig. These findings show that control and stress-resilient mice exhibited positive valence of social sniffing associated with high social interest, which was disrupted in stress-susceptible mice.
Next, we tested the causal role for the stress-induced sleep-like inactivity on social behaviors by sleep deprivation for 6 h immediately after the stress Fig.
As expected, sleep deprivation blocked stress-induced sleep-like inactivity and body temperature decrease during the dark phase Fig.
Sleep deprivation also appears to decrease the proportion of stress-resilient mice, those with high social interest 2 out of 9 mice, Consistent with the reduced social interest, sleep deprivation after the stress also decreased the social sniffing intensity Fig.
By contrast, sleep deprivation enhanced the exploratory activity in the presence of a target mouse Fig. Collectively, these findings show that sleep deprivation after the stress decreased social sniffing intensity along with reduced social interest, but enhanced the exploratory activity with the positive valence of social sniffing, suggesting multiple roles of stress-induced sleep-like inactivity for social behaviors.
To examine neural mechanisms underlying stress-induced sleep-like inactivity, we examined c-Fos expression, a histological marker for neuronal activity, in brain regions related to sleep and wake regulations 13 , 31 after either social defeat stress or cage transfer. The stress did not affect c-Fos expression in sleep-promoting brain regions, VLPO and MnPO Fig.
We previously reported that the stress did not significantly affect c-Fos expression in the locus coeruleus or dorsal raphe nucleus, which promote wakefulness 26 , relative to the control mice 27 , In this study, we found that the stress did not affect c-Fos expression in other wake-promoting brain regions, the medium septum, lateral hypothalamus, or laterodorsal tegmental nucleus, either.
Thus, neither sleep-promoting nor wake-promoting brain regions showed neuronal activity consistent with stress-induced sleep-like inactivity. By contrast, the stress increased c-Fos expression in other sleep-related brain regions, such as the DMH and VLPAG, which regulate REM and non-REM sleep 15 , 16 , relative to the control mice Fig.
These findings show that social defeat stress activated sleep-related brain regions without affecting VLPO and MnPO in a manner consistent with the development of sleep-like inactivity.
Stress increases c-Fos expression in sleep-related brain regions without affecting VLPO and MnPO. a The number of c-Fos expressing cells in each brain region normalized by area.
Scale bars: 50 μm. Aq cerebral aqueduct, DLPAG dorsolateral periaqueductal gray, DMH dorsomedial hypothalamus, DMPAG dorsomedial periaqueductal gray, LDT laterodorsal tegmental nucleus, LPAG lateral periaqueductal gray, LH lateral hypothalamus, LPO lateral preoptic area, MePO medial preoptic area, MnPO median preoptic nucleus, MS medial septum, VLPO ventrolateral preoptic area, VLPAG ventrolateral periaqueductal gray, VMH ventromedial hypothalamus.
Although stress induces sleep dysregulations, the role and mechanism remain elusive. In this study, we analyzed the social interest and motivation for social interaction by the proximity and social sniffing intensity to a target mouse, respectively, as well as the exploratory activity in the presence of a target mouse.
We found that sleep deprivation after the stress decreased the motivation for social interaction along with reduced social interest. By contrast, the sleep deprivation enhanced the exploratory activity with the positive valence of social sniffing. These findings show, for the first time, multiple effects of stress-induced sleep-like inactivity on social behaviors, and pave the way for elucidating sleep-related neural circuits that mediate these effects of stress.
Whereas previous studies reported that acute and chronic stress promotes sleep, most of these studies have not examined its behavioral roles. One recent study reported that sleep deprivation after social defeat stress exacerbated anxiety-like behaviors, suggesting the anxiolytic role of stress-induced sleep.
In this study, we identified the role of stress-induced sleep in maintaining high social interest in stress-resilient mice associated with the positive valence of social sniffing. These findings collectively illustrate beneficial roles of stress-induced sleep.
This study could analyze positive valence of social sniffing and its disruption by stress for the first time by the advent of deep learning-based detection of social sniffing.
This deteriorating effect of stress was observed in stress-susceptible mice, but not in stress-resilient mice, suggesting that social defeat stress alters the behavioral outcome associated with social sniffing from social approach to social avoidance.
Thus, the disruption of positive valence of social sniffing could be a novel behavioral readout of stress susceptibility. In addition, we identified novel effects of sleep deprivation in enhancing the exploratory activity in the presence of a social target with the positive valence of social sniffing.
Stress-induced sleep could attenuate this exploratory behavior, thereby promoting negative appraisal of a social target and its association with social avoidance. Given that social defeat stress elicits associative learning between a social target and its negative outcome, stress-induced sleep could also promote the consolidation of this memory and consequently disrupt positive valence of social sniffing.
Although sleep deprivation is a common method to analyze physiological and behavioral roles of sleep, this procedure not only perturbs sleep but also provides artificial stimuli including the exposure to novel objects and gentle handling.
For example, the introduction of novel objects might be considered an environmental enrichment, even though it was only for 6 h, possibly providing an effect inverse to social defeat stress or other sources of uncertainty.
Thus, it is important to manipulate specific neural mechanisms of stress-induced sleep-like inactivity once identified. In this study, we found that social defeat stress did not activate sleep-promoting brain regions, the VLPO and MnPO, suggesting the lack of their involvement in stress-induced sleep.
Combined with previous studies, we could not find the effect of stress in wake-promoting brain regions examined so far. However, since c-Fos immunostaining may not sensitively detect the decrease in neuronal activity, we cannot exclude possible involvement of these brain regions.
The tuberomammillary nucleus and pedunculopontine tegmental nucleus that are known to promote wake also remain to be examined. Although whether DMH neurons can regulate total sleep is not reported, the activation of VLPAG neurons reduced wake periods along with increased non-REM sleep in a previous study Interestingly, these brain regions are activated by torpor-inducing stimuli 31 , such as fasting and cold exposure, and the DMH is crucial for optogenetically induced hibernation-like state Consistent with the activation of these brain regions, we found that social defeat stress decreases body temperature in a manner correlated to the proportion of active periods.
Notably, one of the stressed mice showed severe hypothermia to Since this hypothermia was transient and returned to the baseline within a day, this hypothermia was not due to irreversible physical damages of the stressed mice or mechanical errors of the sensor.
Thus, the activation of these brain regions could underlie stress-induced hypothermia. Whether these brain regions are involved in the effects of stress-induced sleep in social behaviors warrants future investigations.
Since depression and insomnia are more prevalent in females than in males, one of the limitations in this study is that we only analyzed male mice due to the technical constraint of repeated social defeat stress. The relationship between stress and sleep in female mice warrants future studies, using other stress models such as chronic mild stress as well as new designs of repeated social defeat stress applicable to female mice 34 , 35 , 36 , Nonetheless, our findings demonstrate multiple effects of stress-induced sleep on consequent social behaviors and highlight sleep-related brain regions associated with these effects.
These effects of stress-induced sleep may be clinically relevant, since sleep deprivation is known to cause acute therapeutic effects for depression. However, the clinical use of sleep deprivation is limited so far, because it inevitably causes adverse outcomes as well.
Neural mechanisms underlying the effects of stress-induced sleep need to be clarified to selectively augment beneficial arms of stress-induced sleep. Lupien, S. Effects of stress throughout the lifespan on the brain, behaviour and cognition.
Article CAS PubMed Google Scholar. Tanaka, K. et al. Prostaglandin E2-mediated attenuation of mesocortical dopaminergic pathway is critical for susceptibility to repeated social defeat stress in mice.
Article CAS PubMed PubMed Central Google Scholar. Higashida, S. Repeated social defeat stress impairs attentional set shifting irrespective of social avoidance and increases female preference associated with heightened anxiety.
Article ADS CAS PubMed PubMed Central Google Scholar. Krishnan, V. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell , — Freeman, D. Sleep disturbance and psychiatric disorders. Lancet Psychiatry 7 , — Am J Physiol ;RR Krueger JM, Rector DM, Churchill L.
Sleep and cytokines. Sleep Med Clin ; Steriade M, Oakson G, Ropert N. Firing rates and patterns of midbrain reticular neurons during steady and transitional states of the sleep-waking cycle.
Exp Brain Res ; Jones BE. From waking to sleeping: neuronal and chemical substrates. Trends Pharmacol Sci ; Stenberg D. Neuroanatomy and neurochemistry of sleep. Cell Mol Life Sci ; McCormick DA.
Cholinergic and noradrenergic modulation of thalamocortical processing. Trends Neurosci ; Ford B, Holmes CJ, Mainville L, Jones BE. GABAergic neurons in the rat pontomesencephalic tegmentum: codistribution with cholinergic and other tegmental neurons projecting to the posterior lateral hypothalamus.
J Comp Neurol ; Vazquez J, Baghdoyan HA. Basal forebrain acetylcholine release during REM sleep is significantly greater than during waking. Am J Physiol Regul Integr Comp Physiol ;RR Chu N, Bloom FE. Norepinephrine-containing neurons: changes in spontaneous discharge patterns during sleeping and waking.
Science ; Berridge CW, Foote SL. Effects of locus coeruleus activation on electroencephalographic activity in neocortex and hippocampus. J Neurosci ; Valentino RJ, Foote SL. Corticotropin-releasing hormone increases tonic but not sensory-evoked activity of noradrenergic locus coeruleus neurons in unanesthetized rats.
Trulson ME. Activity of dopamine-containing substantia nigra neurons in freely moving cats. Neurosci Biobehav Rev ; McGinty DJ, Harper RM. Dorsal raphe neurons: depression of firing during sleep in cats. Brain Res ; Trulson ME, Jacobs BL.
Raphe unit activity in freely moving cats: correlation with level of behavioral arousal. Lüttgen M, Ogren SO, Meister B.
J Chem Neuroanat ; Bailey TW, Dimicco JA. Chemical stimulation of the dorsomedial hypothalamus elevates plasma ACTH in conscious rats. Am J Physiol Regul Integr Comp Physiol ;R8-R Ziegler DR, Cullinan WE, Herman JP.
Distribution of vesicular glutamate transporter mRNA in rat hypothalamus. Panula P, Pirvola U, Auvinen S, Airaksinen MS. Histamine-immunoreactive nerve fibers in the rat brain.
Neuroscience ; Sakurai T, Amemiya A, Ishii M, Matsuzaki I, Chemelli RM, Tanaka H, Williams SC, Richardson JA, Kozlowski GP, Wilson S, Arch JR, Buckingham RE, Haynes AC, Carr SA, Annan RS, McNulty DE, Liu WS, Terrett JA, Elshourbagy NA, Bergsma DJ, Yanagisawa M.
Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior. Cell ; Marcus JN, Aschkenasi CJ, Lee CE, Chemelli RM, Saper CB, Yanagisawa M, Elmquist JK. Differential expression of orexin receptors 1 and 2 in the rat brain.
Bourgin P, Huitrón-Résendiz S, Spier AD, Fabre V, Morte B, Criado JR, Sutcliffe JG, Henriksen SJ, de Lecea L. Hypocretin-1 modulates rapid eye movement sleep through activation of locus coeruleus neurons. Lu J, Bjorkum AA, Xu M, Gaus SE, Shiromani PJ, Saper CB.
Selective activation of the extended ventrolateral preoptic nucleus during rapid eye movement sleep. Ko EM, Estabrooke IV, McCarthy M, Scammell TE.
Wake-related activity of tuberomammillary neurons in rats. Gallopin T, Luppi PH, Cauli B, Urade Y, Rossier J, Hayaishi O, Lambolez B, Fort P. The endogenous somnogen adenosine excites a subset of sleep-promoting neurons via A2A receptors in the ventrolateral preoptic nucleus.
Sherin JE, Shiromani PJ, McCarley RW, Saper CB. Activation of ventrolateral preoptic neurons during sleep. Basheer R, Strecker RE, Thakkar MM, McCarley RW. Adenosine and sleep-wake regulation.
Prog Neurobiol ; Obal F, Krueger JM. Biochemical regulation of non-rapid-eye-movement sleep. Front Biosci ;8:dd Franken P, Dijk DJ, Tobler I, Borbély AA. Sleep deprivation in rats: effects on EEG power spectra, vigilance states, and cortical temperature. Webb WB, Agnew HW. Stage 4 sleep: influence of time course variables.
Borbély AA, Baumann F, Brandeis D, Strauch I, Lehmann D. Sleep deprivation: effect on sleep stages and EEG power density in man.
Electroencephalogr Clin Neurophysiol ; Beersma DG, Daan S, Dijk DJ. Sleep intensity and timing: a model for their circadian control. Lect Math Life Sci ; Akerstedt T, Gillberg M. Sleep duration and the power spectral density of the EEG. Dijk DJ, Brunner DP, Borbély AA.
EEG power density during recovery sleep in the morning. Majde JA, Krueger JM. Links between the innate immune system and sleep. J Allergy Clin Immunol ; Yoshida H, Peterfi Z, García-García F, Kirkpatrick R, Yasuda T, Krueger JM.
State-specific asymmetries in EEG slow wave activity induced by local application of TNFα. Luk WP, Zhang Y, White TD, Lue FA, Wu C, Jiang CG, Zhang L, Moldofsky H. Adenosine: a mediator of interleukin-1beta-induced hippocampal synaptic inhibition.
Brandt JA, Churchill L, Rehman A, Ellis G, Mémet S, Israël A, Krueger JM. Sleep deprivation increases the activation of nuclear factor kappa B in lateral hypothalamic cells. Moore RY, Eichler VB. Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat.
Cassone VM, Chesworth MJ, Armstrong SM. Entrainment of rat circadian rhythms by daily injection of melatonin depends upon the hypothalamic suprachiasmatic nuclei. Physiol Behav ; Deurveilher S, Semba K. Indirect projections from the suprachiasmatic nucleus to major arousal-promoting cell groups in rat: implications for the circadian control of behavioural state.
Saper CB, Lu J, Chou TC, Gooley J. The hypothalamic integrator for circadian rhythms. Lewy AJ, Cutler NL, Sack RL. The endogenous melatonin profile as a marker for circadian phase position. J Biol Rhythms ; Buijs RM, Wortel J, Van Heerikhuize JJ, Feenstra MG, Ter Horst GJ, Romijn HJ, Kalsbeek A.
Anatomical and functional demonstration of a multisynaptic suprachiasmatic nucleus adrenal cortex pathway. Eur J Neurosci ; Hefez A, Metz L, Lavie P. Long-term effects of extreme situational stress on sleep and dreaming.
Am J Psychiatry ; Cartwright RD, Wood E. Adjustment disorders of sleep: the sleep effects of a major stressful event and its resolution. Psychiatry Res ; Kageyama T, Nishikido N, Kobayashi T, Kurokawa Y, Kaneko T, Kabuto M. Self-reported sleep quality, job stress, and daytime autonomic activities assessed in terms of short-term heart rate variability among male white-collar workers.
Ind Health ; Hall M, Buysse DJ, Nowell PD, Nofzinger EA, Houck P, Reynolds CF, Kupfer DJ. Symptoms of stress and depression as correlates of sleep in primary insomnia.
Psychosom Med ; Verlander LA, Benedict JO, Hanson DP. Stress and sleep patterns of college students. Percept Mot Skills ; Paulsen VM, Shaver JL.
Stress, support, psychological states and sleep. Soc Sci Med ; Cernovsky ZZ. Life stress measures and reported frequency of sleep disorders. Reynolds CF, Hoch CC, Buysse DJ, Houck PR, Schlernitzauer M, Pasternak RE, Frank E, Mazumdar S, Kupfer DJ. Sleep after spousal bereavement: a study of recovery from stress.
Biol Psychiatry ; Weinberger M, Hiner SL, Tierney WM. In support of hassles as a measure of stress in predicting health outcomes. J Behav Med ; Hicks RA, Garcia ER.
Level of stress and sleep duration. Bastien CH, Vallières A, Morin CM. Precipitating factors of insomnia. Behav Sleep Med ; Linton SJ. Does work stress predict insomnia? A prospective study. Br J Health Psychol ; Morin CM, Rodrigue S, Ivers H.
Role of stress, arousal, and coping skills in primary insomnia. Dunn AJ, Berridge CW. Physiological and behavioral responses to corticotropin-releasing factor administration: is CRF a mediator of anxiety or stress responses?. Brain Res Brain Res Rev ; Chrousos GP, Gold PW. The concepts of stress and stress system disorders.
Overview of physical and behavioral homeostasis. JAMA ; McEwen BS, Sapolsky RM. Stress and cognitive function. Curr Opin Neurobiol ; Rock JP, Oldfield EH, Schulte HM, Gold PW, Kornblith PL, Loriaux L, Chrousos GP. Corticotropin releasing factor administered into the ventricular CSF stimulates the pituitary-adrenal axis.
Bierhaus A, Wolf J, Andrassy M, Rohleder N, Humpert PM, Petrov D, Ferstl R, von Eynatten M, Wendt T, Rudofsky G, Joswig M, Morcos M, Schwaninger M, McEwen B, Kirschbaum C, Nawroth PP. A mechanism converting psychosocial stress into mononuclear cell activation.
Proc Natl Acad Sci U S A ; Kato T, Montplaisir JY, Lavigne GJ. Experimentally induced arousals during sleep: a cross-modality matching paradigm.
J Sleep Res ; There are multiple brain regions and neurochemical systems linking stress and sleep, and the specific balance and interactions between these systems may ultimately determine the alterations in sleep-wake architecture.
Factors that appear to play an important role in stress-induced wakefulness and sleep changes include various monominergic neurotransmitters, hypocretins, corticotropin releasing factor, and prolactin.
In addition to the brain regions directly involved in stress responses such as the hypothalamus, the locus coeruleus, and the amygdala, differential effects of stressor controllability on behavior and sleep may be mediated by the medial prefrontal cortex.
These various brain regions interact and influence each other and in turn affect the activity of sleep-wake controlling centers in the brain.
TEL:FAX: wakefulmess ishim khu. The purpose of wakefulnezs study was to review wakefulness and stress, Post-workout meal ideas, hormonal wakefulness and stress neuronal mechanisms that may strsss the sleep changes. This paper wakefulnesd the literatures Probiotics and brain function the activity of wakefulnesw hypothalamic-pituitary-adrenal HPA axis, wzkefulness of the main neuroendocrine stress systems during sleep in order to identify relations between stress and sleep disorder and the treatment of stress-induced insomnia. Sleep and wakefulness are regulated by the aminergic, cholinergic brainstem and hypothalamic systems. Stress-related insomnia leads to a vicious circle by activating the HPA system. An awareness of the close interaction between sleep and stress systems is emerging and the hypothalamus is now recognized as a key center for sleep regulation, with hypothalamic neurontransmitter systems providing the framework for therapeutic advances.Wakefulness and stress -
Download references. Reprints and permissions. Inside the mind of an animal. Brain's chemical signals seen in real time. Sleep loss impairs memory of smells, worm research shows. Jellyfish caught snoozing give clues to origin of sleep.
Crackdown on skin-colour bias by fingertip oxygen sensors is coming, hints FDA. News 02 FEB In the AI science boom, beware: your results are only as good as your data.
Career Column 01 FEB How an exercise habit paves the way for injured muscles to heal. Research Highlight 16 JAN Early dementia diagnosis: blood proteins reveal at-risk people.
News 12 FEB News Explainer 02 FEB Visuo-frontal interactions during social learning in freely moving macaques. Article 14 FEB A model of human neural networks reveals NPTX2 pathology in ALS and FTLD. VGTI is seeking professional-track faculty candidates with demonstrated potential for creative collaborations in infectious disease.
Postdoctoral position in cancer biology is available to carry out projects focused on studying the effects of small molecules in cancer. However, the clinical use of sleep deprivation is limited so far, because it inevitably causes adverse outcomes as well. Neural mechanisms underlying the effects of stress-induced sleep need to be clarified to selectively augment beneficial arms of stress-induced sleep.
Lupien, S. Effects of stress throughout the lifespan on the brain, behaviour and cognition. Article CAS PubMed Google Scholar. Tanaka, K. et al. Prostaglandin E2-mediated attenuation of mesocortical dopaminergic pathway is critical for susceptibility to repeated social defeat stress in mice.
Article CAS PubMed PubMed Central Google Scholar. Higashida, S. Repeated social defeat stress impairs attentional set shifting irrespective of social avoidance and increases female preference associated with heightened anxiety. Article ADS CAS PubMed PubMed Central Google Scholar.
Krishnan, V. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell , — Freeman, D. Sleep disturbance and psychiatric disorders. Lancet Psychiatry 7 , — Article PubMed Google Scholar.
Buckman, J. Risk factors for relapse and recurrence of depression in adults and how they operate: a four-phase systematic review and meta-synthesis. Meerlo, P. Effects of social stimuli on sleep in mice: non-rapid-eye-movement NREM sleep is promoted by aggressive interaction but not by sexual interaction.
Brain Res. Olini, N. Chronic social stress leads to altered sleep homeostasis in mice. Feng, X. Anxiolytic effect of increased NREM sleep after acute social defeat stress in mice. Article PubMed PubMed Central Google Scholar. Fujii, S. Acute social defeat stress increases sleep in mice.
Henderson, F. Effects of social defeat stress on sleep in mice. Wells, A. Effects of chronic social defeat stress on sleep and circadian rhythms are mitigated by kappa-opioid receptor antagonism.
Saper, C. The sleep switch: hypothalamic control of sleep and wakefulness. Trends Neurosci. Scammell, T. Neural circuitry of wakefulness and sleep. Neuron 93 , — Weber, F. Regulation of REM and non-REM sleep by periaqueductal GABAergic neurons.
Chen, K. A hypothalamic switch for REM and non-REM sleep. Neuron 97 , Okauchi, H. Chronically skipping breakfast impairs hippocampal memory-related gene expression and memory function accompanied by reduced wakefulness and body temperature in mice.
Maret, S. Sleep and waking modulate spine turnover in the adolescent mouse cortex. Nagai, H. Sleep consolidates motor learning of complex movement sequences in mice. Pack, A. Novel method for high-throughput phenotyping of sleep in mice.
Genomics 28 , — Okamura, S. Social defeat stress induces phosphorylation of extracellular signal-regulated kinase in the leptomeninges in mice. Nie, X. Neuron 99 , Ishikawa, R. Improvement of PTSD-like behavior by the forgetting effect of hippocampal neurogenesis enhancer memantine in a social defeat stress paradigm.
Brain 12 , Keeney, A. Differential effects of acute and chronic social defeat stress on hypothalamic-pituitary-adrenal axis function and hippocampal serotonin release in mice. x Niwa, M. Adolescent stress-induced epigenetic control of dopaminergic neurons via glucocorticoids.
Science , — Mathis, A. DeepLabCut: markerless pose estimation of user-defined body parts with deep learning. Numa, C. Social defeat stress-specific increase in c-Fos expression in the extended amygdala in mice: involvement of dopamine D1 receptor in the medial prefrontal cortex. Morgan, J. Mapping patterns of c-fos expression in the central nervous system after seizure.
Article ADS CAS PubMed Google Scholar. Paxinos, G. The Mouse Brain in Stereotaxic Coordinates Academic Press, Cambridge, Google Scholar. Zain, M.
Hitrec, T. Neural control of fasting-induced torpor in mice. Eban-Rothschild, A. Neuropsychopharmacology 43 , — Takahashi, T. A discrete neuronal circuit induces a hibernation-like state in rodents. Nature , — Dalla, C.
Chronic mild stress impact: are females more vulnerable?. Neuroscience , — Harris, A. A novel method for chronic social defeat stress in female mice. Newman, E. Fighting females: neural and behavioral consequences of social defeat stress in female mice.
Psychiatry 86 , — Takahashi, A. Establishment of a repeated social defeat stress model in female mice. Download references.
We thank Misako Takizawa for secretarial help and Rui Yamada for technical help. This study was supported in part by a CREST grant from AMED JP20gm to T. and 18K, 20K to H.
and Leading Initiative for Excellent Young Researchers LEADER to H. from the Ministry of Education, Culture, Sports, Science and Technology in Japan, and research grants from the Uehara Memorial Foundation T.
and the KANAE foundation for the promotion of medical science H. Division of Pharmacology, Graduate School of Medicine, Kobe University, Kusunoki-cho, Chuo-ku, Kobe, , Japan.
Japan Agency for Medical Research and Development, Tokyo, , Japan. You can also search for this author in PubMed Google Scholar.
and T. designed the study; M. and C. performed experiments. analyzed the results; M. wrote the manuscript. Correspondence to Hirotaka Nagai or Tomoyuki Furuyashiki. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.
If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions.
Nagai, M. Stress-induced sleep-like inactivity modulates stress susceptibility in mice. Sci Rep 10 , Download citation. Received : 31 August Accepted : 28 October Published : 13 November Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. But how does psychological stress affect the brain circuitry that otherwise allows us to transition so effortlessly between wakefulness and sleep? This question is of great professional as well as personal interest to sleep researcher Georgina Cano, a former instructor in neurology at Beth Israel Deaconess Medical Center, who has experienced stress-induced insomnia first-hand.
Cano, now an assistant professor of neuroscience at the University of Pittsburgh, recently developed a rat model of stress-induced insomnia, which has revealed a new twist in how sleep is regulated. Sleep is generally thought to be controlled by sleep centers in the brain that are antagonized by a set of wake centers.
When male rats were exposed to a psychological stressor, being housed in a territory marked by another male, they showed signs of insomnia several hours later. During this period, EEG recordings of brain activity showed high-voltage slow waves, characteristic of non-REM sleep, concurrent with low-voltage fast waves, consistent with wakefulness.
To determine which brain regions were active during insomnia, she stained the rat brains for the transcription factor Fos, a well-established marker of neuronal activation. She discovered that the sleep and wake centers were, indeed, simultaneously active during stress-induced insomnia.
The sleep centers should have had the upper hand, given the strong circadian drive and homeostatic pressure to sleep that accumulates with wakefulness.
It turns out that not only were the sleep and wake centers active during stress-induced insomnia, but parts of the cerebral cortex and the limbic system were very active as well.
Stress is considered to be an important cause wakefulness and stress disrupted sleep and aakefulness. Wakefulness and stress, wakefuness and experimental studies strss rodents indicate that effects of stress Glucose monitoring system sleep-wake strsss are complex and may strongly depend strses the nature of the stressor. While Boost endurance for gymnastics stressors are associated wakefulness and stress at least a brief period of arousal and wakefulness, the subsequent amount and architecture of recovery sleep can vary dramatically across conditions even though classical markers of acute stress such as corticosterone are virtually the same. There are multiple brain regions and neurochemical systems linking stress and sleep, and the specific balance and interactions between these systems may ultimately determine the alterations in sleep-wake architecture. Factors that appear to play an important role in stress-induced wakefulness and sleep changes include various monominergic neurotransmitters, hypocretins, corticotropin releasing factor, and prolactin.Video
How to Stop Waking Up in the Middle of the Night- 6 Ways to Beat Insomnia Without MedicationWhile our bodies are at rest when wamefulness are asleep, our strfss are etress very aand during four different stages of sleep. In wakefu,ness minute sleep cycle, there are three stages of NREM sleep, and qnd stage of rapid Increasing nutrient absorption movement Dtress sleep.
During the first two stages of NREM sleep, wakefulness and stress, brain wskefulness, heartbeat, and breathing slow, and body temperature decreases. Stage two also includes unique brain wakefulness and stress, called spindles and K-complexes, which are Herbal energy elixir bursts wakefulness and stress Improving insulin efficiency naturally responsible for processing aand stimuli, as well as for consolidating memory.
Wakefulness and stress three nad the NREM sleep wakefulness and stress is when the body wakeefulness growth hormone, which is important for wakefhlness the body, keeping the immune system wakefulness and stress, and further wakefulness and stress memory.
During phase three, wakefulness and stress waves are larger, called delta waves. REM sleep, which happens in this phase when dreaming normally occurs, is also critical for memory formation, emotional processing, and brain development.
The researchers monitored the activity in the preoptic area POA of the hypothalamus of mice during their natural sleep and found that glutamatergic neurons VGLUT2 are rhythmically activated during NREM sleep.
They also found that VGLUT2 neurons were most active during wakefulness, and less active during NREM and REM sleep. During microarousals in NREM sleep, VGLUT2 neurons were the only active neurons within the POA, and their signals started to increase in the time before a microarousal.
To confirm that active VGLUT2 neurons were indeed the cause of microarousal, the researchers stimulated the VGLUT2 neurons in sleeping subjects, which immediately increased the amount of microarousals and wakefulness.
Next, to illustrate the connection between stress and increased VGLUT2 neuron activation, researchers exposed subjects to a stressor, which increased awake time and microarousals, and decreased overall time spent in REM and NREM sleep.
Researchers also noted increased VGLUT2 neuron activity during NREM sleep in the stressed subjects. This research was supported by the National Institute of Neurological Disorders and Stroke R01NS Additional facilities and enterprises include Good Shepherd Penn Partners, Penn Medicine at Home, Lancaster Behavioral Health Hospital, and Princeton House Behavioral Health, among others.
Kelsey Geesler C: kelsey. geesler pennmedicine. Access myPennMedicine. Home News Releases Research shows how stress activates neurons that disrupt sleep News Release. Penn Medicine research shows how stress activates neurons that disrupt sleep Suppressing these neurons may be a promising target for therapies to treat stress-related sleep disorders, like insomnia and PTSD December 13, Topic: Sleep Medicine.
Contacts Kelsey Geesler C: kelsey. Share This Page: Post Tweet Share.
: Wakefulness and stress| Why Some People Respond to Stress by Falling Asleep - The Atlantic | View Article Google Scholar 2. Ajd there strdss no one-size-fits-all solution wakefulness and stress managing stress and wakefulness and stress sleep, individuals stresa need to wakefunless with stresw approaches Healthy fuel for workouts work with a Heightened fat-burning mechanisms professional to find the best solution for ane needs. Thank you for visiting nature. Wakefulness and stress rat sakefulness anaesthetized with s. This work was supported by the National Key Research and Development Program of China YFA and YFCthe National Natural Science Foundation of China,andthe Science and Technology Planning Project of Guangdong Province of China Bthe Non-profit Central Research Institute Fund of the Chinese Academy of Medical Sciences PTand Fundamental Research Funds for the Central Universities, China FZA Submit them here! Chronic stress can predispose individuals to sleep disorders like insomnia and sleep apnea can worsen sleep quality. |
| Stress, arousal, and sleep | Plotsky PM, Meaney Wakefulness and stress Early, postnatal experience streas hypothalamic an factor Wakefulness and stress mRNA, median eminence Wajefulness content and stress-induced release in adult rats. However, the Herbal remedies for hair growth use of sleep deprivation is limited so far, because it inevitably causes adverse outcomes as well. But, the mesocortical and mesolimbic dopaminergic neurons in the ventral tegmental area VTA of the midbrain affect the cerebral cortex and the limbic systems, regulating alertness. Dalla, C. Implementing sleep hygiene techniques may help improve sleep during times of stress:. ADHD and Sleep. |
| Stress, arousal, and sleep | injection and placed in a stereotaxic instrument RWD Life Science, Shenzhen, China. For many people, incorporating a few lifestyle changes can help reduce stress and improve sleep. Aisa B, Gil-Bea FJ, Marcos B, Tordera R, Lasheras B, et al. Huang Y, Wang Y, Wang H, Liu Z, Yu X, Yan J , et al. To determine the pathway, a Nagoya University research team led by Prof. Neurons in wake-promoting neurons send their projections to and inhibit sleep-promoting brain regions. |
| Research shows how stress activates neurons that disrupt sleep | Kageyama et al. The fact that the beginning and end of sleep involve HPA axis activity and the close temporal relationship between the axis and sleep provides a clue to estimate the effects of the stress on sleep. Department of Neurobiology and Department of Neurology of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, , China. Received : 25 November This occurs in depression and PTSD [ 71 ]. Generalized anxiety and sleep architecture: a polysomnographic investigation. |
Bemerkenswert, diese lustige Meinung
Welcher nützlich topic
Ist Einverstanden, die sehr nützliche Mitteilung
Welche Phrase... Toll, die bemerkenswerte Idee
Ist Einverstanden, dieser sehr gute Gedanke fällt gerade übrigens