Sleep quality and hypertension in an indigenous African population: a cross-sectional investigation from the COMBAT-CVDs study
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Central amygdala somatostatin neurons modulate stress-induced sleep-onset insomnia
Sleep-onset insomnia, characterized by difficulty falling asleep, is linked to increased health risks. Previous studies have shown that the central amygdala (CeA) plays a crucial role in stress regulation, with the somatostatin neurons in the CeA (CeASST+) involved in adaptive stress responses. However, the role of CeASST+ neurons in stress-induced sleep-onset insomnia remains unclear. In this study, we found that the activity of CeASST+ neurons is closely associated with stressful events using fiber photometry in mice. Acute optogenetic activation of CeASST+ neurons induced a rapid transition from non-rapid eye movement (NREM) sleep to wakefulness. Semi-chronic optogenetic and chemogenetic activation of CeASST+ neurons led to prolonged sleep-onset latency and increased wakefulness. Chemogenetic inhibition of these neurons ameliorated sleep-onset insomnia induced by stressful stimuli, but did not affect sleep-wake behavior under physiological conditions. Collectively, our results suggested that CeASST+ neurons are a key neural substrate for modulating stress-induced sleep-onset insomnia, without influencing physiological sleep. These findings highlight CeASST+ neurons as a promising target for treating stress-related sleep-onset insomnia in clinical practice.
The individual determinants of morning dream recall
Evidence suggests that (almost) everyone dreams during their sleep and may actually do so for a large part of the night. Yet, dream recall shows large interindividual variability. Understanding the factors that influence dream recall is crucial for advancing our knowledge regarding dreams’ origin, significance, and functions. Here, we tackled this issue by prospectively collecting dream reports along with demographic information and psychometric, cognitive, actigraphic, and electroencephalographic measures in 217 healthy adults (18–70 y, 116 female participants, 101 male participants). We found that attitude towards dreaming, proneness to mind wandering, and sleep patterns are associated with the probability of reporting a dream upon morning awakening. The likelihood of recalling dream content was predicted by age and vulnerability to interference. Moreover, dream recall appeared to be influenced by night-by-night changes in sleep patterns and showed seasonal fluctuations. Our results provide an account for previous observations regarding inter- and intra-individual variability in morning dream recall.
Self-reported hypertension prevalence, risk factors, and knowledge among South Africans aged 24 to 40 years old
Although hypertension is a significant public health burden in South Africa (SA), less is known about its prevalence, risk factors, and possible preventative strategies among young adults. We assessed the prevalence, possible risk factors, and knowledge associated with self-reported hypertension among young adults from SA. A cross-sectional online survey was conducted among 1000 young South African adults (24–40 years; 51.0% women). We administered a socio-demographic questionnaire and collected information on measures of socio-economic status (SES) (e.g. asset wealth index), self-reported medical history, and lifestyle risk factors. Furthermore, a modified version of the hypertension evaluation of lifestyle and management questionnaire was used to assess participants’ hypertension knowledge. The overall prevalence of self-reported hypertension was 24.0%, with significant differences between women and men (27.5% and 20.4% respectively, p = 0.033). Only 16.8% of the respondents had good hypertension knowledge. There was a positive association between good knowledge of hypertension and being hypertensive (OR = 1.43 CI:1.23–3.12), monthly blood pressure check-ups (OR = 2.03 CI:1.78–3.23), knowing the side effects of uncontrolled blood pressure (OR = 1.28 CI:1.07–1.89) and having a biological mother with hypertension (OR = 1.79 CI:1.53–2.21). Being employed full-time (OR = 0.74 CI:0.69–0.80), having a higher SES (wealth index 4 (OR = 0.70 CI:0.59–0.97) and 5 (OR = 0.65 CI:0.48–0.81)), exercising 6 to 7 days per week (OR = 0.83 CI:0.71–0.94), and not consuming alcohol at all (OR = 0.73 CI:0.67–0.89), were all found to be protective against hypertension. The high hypertension prevalence, lack of hypertension knowledge, and reported risk factors among this group highlight the need for early robust preventative strategies to mitigate hypertension risk among this population.
Mettl3-m6A-NPY axis governing neuron–microglia interaction regulates sleep amount of mice
Sleep behavior is regulated by diverse mechanisms including genetics, neuromodulation and environmental signals. However, it remains completely unknown regarding the roles of epitranscriptomics in regulating sleep behavior. In the present study, we showed that the deficiency of RNA m6A methyltransferase Mettl3 in excitatory neurons specifically induces microglia activation, neuroinflammation and neuronal loss in thalamus of mice. Mettl3 deficiency remarkably disrupts sleep rhythm and reduces the amount of non-rapid eye movement sleep. We also showed that Mettl3 regulates neuropeptide Y (NPY) via m6A modification and Mettl3 conditional knockout (cKO) mice displayed significantly decreased expression of NPY in thalamus. In addition, the dynamic distribution pattern of NPY is observed during wake-sleep cycle in cKO mice. Ectopic expression of Mettl3 and NPY significantly inhibits microglia activation and neuronal loss in thalamus, and restores the disrupted sleep behavior of cKO mice. Collectively, our study has revealed the critical function of Mettl3-m6A-NPY axis in regulating sleep behavior.
Raptin, a sleep-induced hypothalamic hormone, suppresses appetite and obesity
Sleep deficiency is associated with obesity, but the mechanisms underlying this connection remain unclear. Here, we identify a sleep-inducible hypothalamic protein hormone in humans and mice that suppresses obesity. This hormone is cleaved from reticulocalbin-2 (RCN2), and we name it Raptin. Raptin release is timed by the circuit from vasopressin-expressing neurons in the suprachiasmatic nucleus to RCN2-positive neurons in the paraventricular nucleus. Raptin levels peak during sleep, which is blunted by sleep deficiency. Raptin binds to glutamate metabotropic receptor 3 (GRM3) in neurons of the hypothalamus and stomach to inhibit appetite and gastric emptying, respectively. Raptin-GRM3 signaling mediates anorexigenic effects via PI3K-AKT signaling. Of note, we verify the connections between deficiencies in the sleeping state, impaired Raptin release, and obesity in patients with sleep deficiency. Moreover, humans carrying an RCN2 nonsense variant present with night eating syndrome and obesity. These data define a unique hormone that suppresses food intake and prevents obesity.
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