The Immediate and Long-lasting Cognitive Consequences of Adolescent Chronic Sleep Restriction

Adolescence is a critical developmental period. An important change that occurs in adolescence is the neurological maturation for adult-type cognitive abilities. Research has linked adequate sleep quantity to successful learning and memory capabilities. However, due to a shift in sleep timing drive in adolescence, in combination with early awakening for school, the adolescent population is experiencing chronic sleep restriction (CSR). What repercussions to long-term memory capabilities could CSR in adolescence have immediately and are the consequences long-lasting? The present study modeled human adolescent CSR in rats through four hours of sleep deprivation for five days, followed by two days of unrestricted sleep, and five more days of four hours of sleep deprivation; thus the rats were exposed to CSR throughout the two-week rat adolescent period. Long-term hippocampal dependent and non-hippocampal dependent memory were tested through the object location task and the object recognition task, respectively. Testing occurred in adolescence and after a four-week delay during which the rats slept freely and matured to adulthood. The results showed that, given the appropriate conditions for successful long-term memory, the rats exposed to CSR in adolescence showed impaired hippocampal dependent memory in adolescence and this impairment was also evident in adulthood. These findings were not the case for non-hippocampal dependent memory, for which a significant effect of sleep was not found. Given the findings of the hippocampal dependent task, these results suggest that CSR in adolescence may influence less than optimal memory performance among adolescents. Further, the pattern in adulthood suggests that even after undisturbed sleep in the period from adolescence to adult maturation, the consequences of adolescent CSR are relentless. The findings in this study inform the research as the first rodent model of adolescent CSR and indicate practical implications for the health of adolescents

Developmental Toxicity of Nicotine: A Transdisciplinary Synthesis and Implications for Emerging Tobacco Products

While the health risks associated with adult cigarette smoking have been well described, effects of nicotine exposure during periods of developmental vulnerability are often overlooked. Using MEDLINE and PubMed literature searches, books, reports and expert opinion, a transdisciplinary group of scientists reviewed human and animal research on the health effects of exposure to nicotine during pregnancy and adolescence. A synthesis of this research supports that nicotine contributes critically to adverse effects of gestational tobacco exposure, including reduced pulmonary function, auditory processing defects, impaired infant cardiorespiratory function, and may contribute to cognitive and behavioral deficits in later life. Nicotine exposure during adolescence is associated with deficits in working memory, attention, and auditory processing, as well as increased impulsivity and anxiety. Finally, recent animal studies suggest that nicotine has a priming effect that increases addiction liability for other drugs. The evidence that nicotine adversely affects fetal and adolescent development is sufficient to warrant public health measures to protect pregnant women, children, and adolescents from nicotine exposure

Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress

Sleep has been ascribed a critical role in cognitive functioning. Several lines of evidence implicate sleep in the consolidation of synaptic plasticity and long-term memory. Stress disrupts sleep while impairing synaptic plasticity and cognitive performance. Here, we discuss evidence linking sleep to mechanisms of protein synthesis-dependent synaptic plasticity and synaptic scaling. We then consider how disruption of sleep by acute and chronic stress may impair these mechanisms and degrade sleep function

Promoting sleep health during pregnancy for enhancing women's health: a longitudinal randomized controlled trial combining biological, physiological and psychological measures, Maternal Outcome after THERapy for Sleep (MOTHERS).

BACKGROUND Sleep is vital for maintaining individuals' physical and mental health and is particularly challenged during pregnancy. More than 70% of women during the gestational period report insomnia symptoms. Sleep dysfunction in the peripartum increases the risk for a cascade of negative health outcomes during late pregnancy, birth, and postpartum. While psychological interventions are considered the first line treatment for sleep difficulties, they are still scarcely offered during pregnancy and there is a lack of longitudinal research combining psychological and physiological indices. METHODS The present protocol outlines a randomized controlled trial aimed at testing the long-term effectiveness of an automatized digitalized psychoeducational intervention for insomnia for expectant mothers complaining insomnia symptoms without comorbidity. Outcomes include physiological, hormonal, and subjective indices of maternal psychopathology, stress, and emotional processes, and sleep and wellbeing of the family system. The trial is part of a longitudinal study evaluating expectant mothers from early pregnancy (within the 15th gestational week) to 6-months postpartum through 6 observational phases: baseline (BSL), 6- and 12-weeks from BSL (FU1-FU2), 2-to-4 weeks after delivery (FU3), and 3- and 6-months after delivery (FU4-5). We plan to recruit 38 women without sleep difficulties (Group A) and 76 women with sleep difficulties (Group B). Group B will be randomly assigned to digital psychological control intervention (B1) or experimental psychoeducational intervention targeting insomnia (B2). At 3 time points, an ecological-momentary-assessment (EMA) design will be used to collect data on sleep and emotions (diaries), sleep-wake parameters (actigraphy) and stress reactivity (salivary cortisol). We will also test the DNA methylation of genes involved in the stress response as biomarkers of prenatal poor sleep. Information on partner's insomnia symptoms and new-borns' sleep will be collected at each stage. DISCUSSION The proposed protocol aims at testing an easily accessible evidence-based psychoeducational intervention for expectant mothers to help them improving sleep, health, and wellbeing in the peripartum. The results could improve the understanding and management of sleep difficulties and peripartum depression. TRIAL REGISTRATION The study protocol has been registered on 22 April 2024 with ClinicalTrials.gov Protocol Registration and Results System (PRS), ID: NCT06379074. PROTOCOL VERSION April 23, 2024

Stress, Monoamines, and Cognitive Flexibility

Stress has been implicated in psychiatric disorders that are characterized by impaired executive function, which is mediated by the prefrontal cortex (PFC). The stress-related neuropeptide, corticotropin-releasing factor (CRF) regulates monoamine systems that project to the PFC, including the locus coeruleus norepinephrine (LC-NE) system and the dorsal raphe-serotonin (DRN-5-HT) system. CRF actions on these systems may underlie cognitive symptoms of stress-related disorders. The age at which stress occurs can determine its impact, and adolescent stress has been linked to adult psychopathology. This dissertation explores the role of CRF in stress-induced modulation of the LC-NE and DRN-5-HT systems and the developmental time course of the impact of stress on PFC-dependent cognitive function using attentional set-shifting tasks, microdialysis, and immunohistochemistry. CRF microinfusion into the LC and DRN produced dose-dependent effects on distinct cognitive functions. Low doses CRF in the LC facilitated set-shifting and increased c-fos expression in the PFC. In contrast, high doses of CRF in the LC facilitated reversal learning, suggesting that mild and severe stress affect different cognitive processes through LC-PFC projections. In the DRN, CRF facilitated set-shifting at a dosage that decreased 5-HT levels in the PFC. This effect switched to facilitation of reversal learning in a defeat-resistant subpopulation of rats exposed to social stress, underscoring the importance of stress history and coping strategy in determining the impact of stress. Finally, adolescent social stress produced an enduring impairment of cognitive flexibility that was seen in adulthood and occurred selectively in rats that resisted social defeat, further reinforcing the importance of coping style in the consequences of stress. Together these studies demonstrate how CRF modulation of monoamine systems can affect cognitive flexibility in ways that are adaptive for dealing with acute stress. They also show the importance of stress history, coping style, and age at which stress occurs as determinants of the impact of stress on cognition. This research may lead to the development of novel, individualized monoamine-targeted treatments for individuals suffering from stress-related cognitive impairments that may be related to the etiology of a diverse range of psychiatric disorders

Sleep and Cognition

Sleep is an ancestral and primitive behaviour, an important part of life thought to be essential for restoration of body and mind. As adults, we spend approximately a third of our lives asleep and as we progress through life there are certain shifts in sleep architecture, most notably in sleep quantity. These biological or physiological age-dependent changes in sleep are well documented [1], and alongside the shifts in sleep architecture there is an increased susceptibility to certain sleep disorders. Sleep disturbances and sleep deprivation are common in modern society. Most studies show that since the beginning of the century, populations have been subjected to a steady constant decline in the number of hours devoted to sleep. This is due to changes in a variety of environmental and social conditions (e.g. less dependence on daylight for most activities, extended shift work and 24/7 round-the-clock activities