The Role of Reproductive Hormones in Sex Differences in Sleep Homeostasis and Arousal Response in Mice.
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ABSTRACT:
SUBMITTER: Choi J
PROVIDER: S-EPMC8491770 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Sleep and wakefulness are not simple, homogenous all-or-none states but represent a spectrum of substates, distinguished by behavior, levels of arousal, and brain activity at the local and global levels. Until now, the role of the hypothalamic circuitry in sleep-wake control was studied primarily with respect to its contribution to rapid state transitions. In contrast, whether the hypothalamus modulates within-state dynamics (state "quality") and the functional significance thereof remains unexplored. Here, we show that photoactivation of inhibitory neurons in the lateral preoptic area (LPO) of the hypothalamus of adult male and female laboratory mice does not merely trigger awakening from sleep, but the resulting awake state is also characterized by an activated electroencephalogram (EEG) pattern, suggesting increased levels of arousal. This was associated with a faster build-up of sleep pressure, as reflected in higher EEG slow-wave activity (SWA) during subsequent sleep. In contrast, photoinhibition of inhibitory LPO neurons did not result in changes in vigilance states but was associated with persistently increased EEG SWA during spontaneous sleep. These findings suggest a role of the LPO in regulating arousal levels, which we propose as a key variable shaping the daily architecture of sleep-wake states.
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Project description:BackgroundOur previous study revealed that adult female rats respond differently to trauma than adult males, recapitulating sex differences in symptoms of post-traumatic stress disorder (PTSD) exhibited by women and men. Here, we asked two questions: does the female phenotype depend on (1) social housing condition and/or (2) circulating gonadal hormones?MethodsFor the first study, the effects of single prolonged stress (SPS) were compared for females singly or pair-housed. For the second study, adult male and female rats were gonadectomized or sham-gonadectomized 2 weeks prior to exposure to SPS, with half the gonadectomized rats given testosterone. In addition to the typical measures of the trauma response in rats, acoustic startle response (ASR), and the dexamethasone suppression test (DST), we also used two other measures typically used to assess depressive-like responses, social interaction and sucrose preference. Glucocorticoid receptor (GR) expression in the hypothalamus was also examined.ResultsWe now report that the distinct trauma response of female rats is not influenced by social housing condition. Moreover, sex differences in the response to SPS based on ASR and DST, replicated in the current study, are independent of adult gonadal hormones. Regardless of hormonal status, traumatized males show a hyper-responsive phenotype whereas traumatized females do not. Moreover, testosterone treatment in adulthood did not masculinize the response to trauma in females. Notably, both sucrose preference and social interaction tests revealed an effect of trauma in females but not in males, with the effects of SPS on sucrose preference dependent on ovarian hormones. Effects of SPS on GR expression in the hypothalamus also depended on gonadal hormones in females.ConclusionsWe propose that the trauma response for female rats is depressive in nature, recapitulating the female bias in PTSD for internalizing symptoms and major depression in contrast to the externalizing symptoms of males. Presumed core markers of PTSD (enhanced ASR and negative feedback control of corticosterone) are apparently relevant only to males and are independent of adult gonadal hormones. Such sex differences in trauma responding are likely determined earlier in life. We conclude that males and females show fundamentally different responses to trauma that do not simply reflect differences in resilience.
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Project description:In all animals, sleep pressure is under continuous tight regulation. It is universally accepted that this regulation arises from a two-process model, integrating both a circadian and a homeostatic controller. Here we explore the role of environmental social signals as a third, parallel controller of sleep homeostasis and sleep pressure. We show that, in Drosophila melanogaster males, sleep pressure after sleep deprivation can be counteracted by raising their sexual arousal, either by engaging the flies with prolonged courtship activity or merely by exposing them to female pheromones.
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Project description:Response to stress is dysregulated in psychosis (PSY). fMRI studies showed hyperactivity in hypothalamus (HYPO), hippocampus (HIPP), amygdala (AMYG), anterior cingulate (ACC), orbital and medial prefrontal (OFC; mPFC) cortices, with some studies reporting sex differences. We predicted abnormal steroid hormone levels in PSY would be associated with sex differences in hyperactivity in HYPO, AMYG, and HIPP, and hypoactivity in PFC and ACC, with more severe deficits in men. We studied 32 PSY cases (50.0% women) and 39 controls (43.6% women) using a novel visual stress challenge while collecting blood. PSY males showed BOLD hyperactivity across all hypothesized regions, including HYPO and ACC by FWE-correction. Females showed hyperactivity in HIPP and AMYG and hypoactivity in OFC and mPFC, the latter FWE-corrected. Interaction of group by sex was significant in mPFC (F = 7.00, p = 0.01), with PSY females exhibiting the lowest activity. Male hyperactivity in HYPO and ACC was significantly associated with hypercortisolemia post-stress challenge, and mPFC with low androgens. Steroid hormones and neural activity were dissociated in PSY women. Findings suggest disruptions in neural circuitry-hormone associations in response to stress are sex-dependent in psychosis, particularly in prefrontal cortex.
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Project description:ContextObesity is known to impact reproductive function in adults, but little is known about its effects on reproductive hormones during puberty.ObjectiveTo assess sex differences in effects of obesity on reproductive hormones and their relation to insulin sensitivity and secretion.DesignCross-sectional study including anthropometrics, serum and urine reproductive hormone concentrations, and intravenous glucose tolerance testing (IVGTT) to assess acute insulin response to glucose (AIRg), and insulin sensitivity (Si).SettingOutpatient academic clinical research center.PatientsGirls (52%) and boys (48%) who were normal weight (NW; n = 51, BMI-Z score = -0.11 ± 0.77, age = 11.5 ± 1.7 years) and obese (n = 53, BMI-Z score = 2.22 ± 0.33, age = 10.9 ± 1.5 years), Tanner stage 2 to 3.ResultsBoys with obesity had lower total testosterone (P < 0.0001) and higher concentrations of the urinary estradiol metabolite, E1c, (P = 0.046) than boys with NW. Girls with obesity had higher free androgen index (FAI; P = 0.03) than NW girls. Both boys and girls with obesity had lower sex hormone-binding globulin (SHBG; P < 0.0001) than NW. AIRg was inversely related to SHBG in boys (R = 0.6, P < 0.0001) and girls (R = 0.53, P = 0.0001). Si correlated with higher SHBG in boys (R2 = 0.67, P < 0.0001) and girls (R = 0.5, P = 0.0003), higher total testosterone for boys (R = 0.39, P = 0.01), and lower FAI for girls (R = -0.2, P = 0.04).ConclusionYouth with obesity have lower SHBG than youth with NW, but obesity has differential effects on reproductive hormones in girls versus boys, which are apparent early in puberty. Ongoing longitudinal studies will evaluate the impact of obesity on reproductive hormones in girls and boys as puberty progresses.
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Project description:To investigate the prevalence of binge viewing, its association with sleep and examine arousal as an underlying mechanism of this association.Four hundred twenty-three adults (aged 18-25 years old, 61.9% female) completed an online survey assessing regular television viewing, binge viewing, sleep quality (Pittsburgh Sleep Quality Index), fatigue (Fatigue Assessment Scale), insomnia (Bergen Insomnia Scale), and pre-sleep arousal (Pre-Sleep Arousal Scale). Regression analyses were conducted. Mediation analysis was performed using PROCESS Macro.There were 80.6% who identified themselves as a binge viewer. Among those who binge viewed (n = 341), 20.2% had binge viewed at least a few times a week during the past month. Among poor sleepers (Pittsburgh Sleep Quality Index > 5), 32.6% had a poor sleep quality associated with being a binge viewer. Higher binge viewing frequency was associated with a poorer sleep quality, increased fatigue and more symptoms of insomnia, whereas regular television viewing was not. Cognitive pre-sleep arousal fully mediated these relationships.New viewing styles such as binge viewing are increasingly prevalent and may pose a threat to sleep. Increased cognitive arousal functions as the mechanism explaining these effects. Measures of media exposure should take into account the user's level of engagement with media. Interventions aimed at (1) alerting viewers about excessive viewing duration and (2) reducing arousal before sleep may be useful ways to tackle sleep problems in binge viewers.
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Project description:Study objectivesTreating ovariectomized rats with physiological levels of estradiol and/or progesterone affects aspects of both baseline (24 h) sleep and recovery (18 h) sleep after 6 h of sleep deprivation. We have extended the analysis of these effects by examining several additional parameters of sleep architecture using the same data set as in our previous study (Deurveilher et al. SLEEP 2009;32(7):865-877).DesignSleep in ovariectomized rats implanted with oil, 17 ?-estradiol and/or progesterone capsules was recorded using EEG and EMG before, during, and after 6 h of sleep deprivation during the light phase of a 12/12 h light/dark cycle.Measurements and resultsDuring the baseline dark, but not light, phase, treatments with estradiol alone or combined with progesterone decreased the mean duration of non-rapid eye movement sleep (NREMS) episodes and the number of REMS episodes, while also increasing brief awakenings, consistent with the previously reported lower baseline NREMS and REMS amounts. Following sleep deprivation, the hormonal treatments caused a larger percentage increase from baseline in the mean durations of NREMS and REMS episodes, and a larger percentage decrease in brief awakenings, consistent with the previously reported larger increase in recovery REMS amount. There were no hormonal effects on NREMS and REMS EEG power values, other than on recovery NREMS delta power, as previously reported.ConclusionsPhysiological levels of estradiol and/or progesterone in female rats modulate sleep architecture differently at baseline and after acute sleep loss, fragmenting baseline sleep while consolidating recovery sleep. These hormones also play a role in the diurnal pattern of NREMS maintenance.
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Project description:Sleep fragmentation (SF) is an integral feature of sleep apnea and other prevalent sleep disorders. Although the effect of repetitive arousals on cognitive performance is well documented, the effects of long-term SF on electroencephalography (EEG) and molecular markers of sleep homeostasis remain poorly investigated. To address this question, we developed a mouse model of chronic SF and characterized its effect on EEG spectral frequencies and the expression of genes previously linked to sleep homeostasis including clock genes, heat shock proteins, and plasticity-related genes.N/A.Animal sleep research laboratory.Sixty-six C57BL6/J adult mice.Instrumental sleep disruption at a rate of 60/h during 14 days.Locomotor activity and EEG were recorded during 14 days of SF followed by recovery for 2 days. Despite a dramatic number of arousals and decreased sleep bout duration, SF minimally reduced total quantity of sleep and did not significantly alter its circadian distribution. Spectral analysis during SF revealed a homeostatic drive for slow wave activity (SWA; 1-4 Hz) and other frequencies as well (4-40 Hz). Recordings during recovery revealed slow wave sleep consolidation and a transient rebound in SWA, and paradoxical sleep duration. The expression of selected genes was not induced following chronic SF.Chronic SF increased sleep pressure confirming that altered quality with preserved quantity triggers core sleep homeostasis mechanisms. However, it did not induce the expression of genes induced by sleep loss, suggesting that these molecular pathways are not sustainably activated in chronic diseases involving SF.
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Project description:The gastrointestinal tract has a crucial role in the control of energy homeostasis through its role in the digestion, absorption, and assimilation of ingested nutrients. Furthermore, signals from the gastrointestinal tract are important regulators of gut motility and satiety, both of which have implications for the long-term control of body weight. Among the specialized cell types in the gastrointestinal mucosa, enteroendocrine cells have important roles in regulating energy intake and glucose homeostasis through their actions on peripheral target organs, including the endocrine pancreas. This article reviews the biological actions of gut hormones regulating glucose homeostasis, with an emphasis on mechanisms of action and the emerging therapeutic roles of gut hormones for the treatment of type 2 diabetes mellitus.
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