Effects of Paradoxical Sleep Deprivation on MCH and Hypocretin Systems.

Melanin-concentrating hormone (MCH) and hypocretins (Hcrt) 1 and 2 are neuropeptides synthesized in the lateral hypothalamic area by neurons that are critical in the regulation of sleep and wakefulness. Their receptors are located in the same cerebral regions, including the frontal cortex and hippocampus. The present study aimed to assess whether 96 hours of paradoxical sleep deprivation alters the functioning of the MCH and hypocretin systems.

Impaired Basal Forebrain Cholinergic Neuron GDNF Signaling Contributes to Perioperative Sleep Deprivation-Induced Chronicity of Postsurgical Pain in Mice Through Regulating Cholinergic Neuronal Activity, Apoptosis, and Autophagy.

Aims: This study investigated the roles of lateral basal forebrain glial cell line-derived neurotrophic factor (GDNF) signaling and cholinergic neuron activity, apoptosis, and autophagy dysfunction in sleep deprivation-induced increased risk of chronic postsurgical pain (CPSP) in mice.

Methods: Sleep deprivation (6 h per day from -1 to 3 days postoperatively) was administered to mice receiving skin/muscle incision and retraction (SMIR) to determine whether perioperative sleep deprivation induces mechanical and thermal pain hypersensitivity, increases the risk of chronic pain, and causes changes of basal forebrain neurons activity (c-Fos immunostaining), apoptosis (cleaved Caspase-3 expression), autophagy (LC3 and p62 expression) and GDNF expression. Adeno-associated virus (AAV)-GDNF was microinjected into the basal forebrain to see whether increased GDNF expression could reverse sleep deprivation-induced changes in pain duration and cholinergic neuron apoptosis and autophagy.

Sleep Deprivation in Healthy Males Increases Muscle Afferents, Impairing Motor Preparation and Reducing Endurance.

Purpose: Sleep deprivation (SD) reduces time to task failure during endurance exercises. The aim of our work was to study the effect of acute SD on the endurance of a skeletal hand muscle and to investigate cortical motor drive to muscle and perception of effort.

Methods: Origin of the early exhaustion after SD might be insufficient cortical motor drive to muscle or motor inhibition because of excessive perception of effort.

[Effect of electroacupuncture on synaptic ultrastructure and synaptic function related proteins PSD95 and MeCP2 in sleep deprivation rats].

Objectives: To observe the effect of electroacupuncture (EA) on the expression of synaptic function related proteins PSD95 and MeCP2 and synaptic ultrastructure in sleep deprived rats, so as to explore its mechanism underlying improvement of learning and memory ability caused by sleep deprivation.

Methods: SD rats were randomly divided into normal, model, EA and sham EA groups (=10). The sleep deprivation model was prepared by modified multi-platform water environment.

Balancing brain metabolic states during sickness and recovery sleep.

Sickness sleep and rebound following sleep deprivation share humoral signals including the rise of cytokines, in particular interleukins. Nevertheless, they represent unique physiological states with unique brain firing patterns and involvement of specific circuitry. Here, we performed untargeted metabolomics of mouse cortex and hippocampus to uncover changes with sickness and rebound sleep as compared with normal daily sleep.

Individualized rTMS Intervention Targeting Sleep Deprivation-Induced Vigilance Decline: Task fMRI-Guided Approach.

Study Objectives: Sleep deprivation (SD) is prevalent in our increasingly round-the-clock society. Optimal countermeasures such as ample recovery sleep are often unfeasible, and brief naps, while helpful, do not fully restore cognitive performance following SD. Thus, we propose that targeted interventions, such as repetitive transcranial magnetic stimulation (rTMS), may enhance cognitive performance recovery post-SD.

Using the Person-Based Approach to Co-Create and Optimize an App-Based Intervention to Support Better Sleep for Adolescents in the United Kingdom: Mixed Methods Study.

Background: Poor sleep is a common problem in adolescents aged 14 to 18 years. Difficulties with sleep have been found to have a bidirectional link to mental health problems.

Objective: This new research sought to involve young people in the co-creation of a new app, particularly those from underserved communities.

A systematic and meta-analytic review of the impact of sleep restriction on memory formation.

Modern life causes a quarter of adults and half of teenagers to sleep for less than is recommended (Kocevska et al., 2021). Given well-documented benefits of sleep on memory, we must understand the cognitive costs of short sleep.

The connection between sleep deficiency and coronary artery disease: Complexities and controversies.

The growing burden of coronary artery disease (CAD) has led to a deeper exploration of the pathophysiologic mechanisms underlying the disease process with the hope of finding novel treatments to reduce CAD morbidity and mortality. Sleep is a normal physiologic phenomenon essential for maintaining homeostasis. Disruption in sleep physiology has been linked to the activation of pro-inflammatory cytokines that may predispose to a greater risk of CAD.

Sleep loss-induced oncogenic pathways are mediated via the neuron-specific interleukin-1 receptor accessory protein (AcPb).

Interleukin-1β (IL1), a pleiotropic cytokine, is involved in sleep regulation, tumor ontogeny, and immune responses. IL1 receptor adaptor proteins, including the IL1 receptor accessory protein (AcP), and its neuron-specific isoform, AcPb, are required for IL1 signaling. The AcPb isoform is resultant from alternate splicing of the AcP transcript.

How to quantify sleepiness during an attempt to sleep?

. Sleepiness assessment tools were mostly developed for detection of an elevated sleepiness level in the condition of sleep deprivation and several medical conditions. However, sleepiness occurs in various other conditions including the transition from wakefulness to sleep during an everyday attempt to get sleep.

Enhanced diversity on connector hubs following sleep deprivation: Evidence from diffusion and functional magnetic resonance imaging.

Sleep deprivation has been demonstrated to exert widespread and intricate impacts on the brain network. The human brain network is a modular network composed of interconnected nodes. This network consists of provincial hubs and connector hubs, with provincial hubs having diverse connectivities within their own modules, while connector hubs distribute their connectivities across different modules.

Transcriptional dynamics of sleep deprivation and subsequent recovery sleep in the male mouse cortex.

Sleep is an essential, tightly regulated biological function. Sleep is also a homeostatic process, with the need to sleep increasing as a function of being awake. Acute sleep deprivation (SD) increases sleep need, and subsequent recovery sleep (RS) discharges it.

Acute partial sleep deprivation attenuates blood pressure responses to cycling exercise.

Exaggerated blood pressure (BP) responses during exercise are independently associated with future development of hypertension. Partial sleep deprivation (PSD) can increase 24-h ambulatory BP, but the effects on exercise BP are unclear. We hypothesized that acute PSD would augment the BP response to constant load cycling exercise and a 20-min time trial.

Circadian rhythm sleep loss impairs motor inhibition more than motor execution in continuous action.

Under total sleep deprivation, both inhibitory and motor control are impaired. However, how circadian rhythm sleep loss caused by irregular sleep pattern affects motor inhibition and execution in continuous actions remains unknown. This study utilized a pointing task to investigate the question over 30 days.

Preliminary investigations into human neurofluid transport using multiple novel non-contrast MRI methods.

We discuss two potential non-invasive MRI methods to study phenomena related to subarachnoid cerebrospinal fluid (CSF) motion and perivascular fluid transport, and their association with sleep and aging. We apply diffusion-based intravoxel incoherent motion (IVIM) imaging to evaluate pseudodiffusion coefficient, , or CSF movement across large spaces like the subarachnoid space (SAS). We also performed perfusion-based multi-echo, Hadamard encoded arterial spin labeling (ASL) to evaluate whole brain cortical cerebral blood flow (CBF) and trans-endothelial exchange () of water from the vasculature into the perivascular space and parenchyma.

CRY2 mediates the cognitive decline induced by sleep deprivation in 5xFAD mice.

Background: Cryptochrome-2 (CRY2) is a core rhythm gene that plays a crucial role in DNA damage repair. The present study investigated the potential role of CRY2 in mediating sleep deprivation-induced cognitive decline in 5xFAD mice.

Methods: To assess the effects of SD on different brain regions of the mouse brain, we used 18F FDG PET-CT.

Sleep deprivation causes gut dysbiosis impacting on systemic metabolomics leading to premature ovarian insufficiency in adolescent mice.

Currently, there are occasional reports of health problems caused by sleep deprivation (SD). However, to date, there remains a lack of in-depth research regarding the effects of SD on the growth and development of oocytes in females. The present work aimed to investigate whether SD influences ovarian folliculogenesis in adolescent female mice.