Humans don't hibernate, but we still need more winter sleep frontiersin
). The fact that the dataset shows a seasonal difference, as opposed to the expected changes, could indicate that these changes may be even greater if generalized to a healthy population. Nevertheless, it was important to carefully account for confounding factors in the patient group. Since certain medications, that are prevalent to be taken by a neuropsychiatric cohort, interfere with sleep in multiple ways, a large number of patients had to be excluded from the analysis.
Seasonal changes in sleep architecture may have implications for recommendations regarding sleep routines. For many people, the time to wake up is more strongly controlled by their employer’s business hours or school times than by their internal clock. Adjustment of sleep schedule can, therefore, only be controlled by choosing the time to go to bed. Nevertheless, keeping to the same time is widely recommended and often enforced religiously on children.
In conclusion, the observed significant change in prolonged REM sleep duration in winter vs. spring was in line with previous studies. The data indicate that sleep architecture in patients with sleep disorders is affected by seasonal changes, even in an urban environment with low natural light exposure and high light pollution.
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Frontiers | Deficiency in the cell-adhesion molecule dscaml1 impairs hypothalamic CRH neuron development and perturbs normal neuroendocrine stress axis functionThe corticotropin-releasing hormone (CRH)-expressing neurons in the hypothalamus are critical regulators of the neuroendocrine stress response pathway, known as the hypothalamic-pituitary-adrenal (HPA) axis. As developmental vulnerabilities of CRH neurons contribute to stress-associated neurological and behavioral dysfunctions, it is critical to identify the mechanisms underlying normal and abnormal CRH neuron development. Using zebrafish, we identified Down syndrome cell adhesion molecule like-1 (dscaml1) as an integral mediator of CRH neuron development and necessary for establishing normal stress axis function. In dscaml1 mutant animals, hypothalamic CRH neurons had higher crhb (the CRH homolog in fish) expression, increased cell number, and reduced cell death compared to wild-type controls. Physiologically, dscaml1 mutant animals had higher baseline stress hormone (cortisol) levels and attenuated responses to acute stressors. Together, these findings identify dscaml1 as an essential factor for stress axis development and suggest that HPA axis dysregulation may contribute to the etiology of human DSCAML1-linked neuropsychiatric disorders.
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