Aerospace Medicine and Biology: A continuing bibliography with indexes

This bibliography lists 253 reports, articles, and other documents introduced into the NASA scientific and technical information system in October 1975

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 125

This special bibliography lists 323 reports, articles, and other documents introduced into the NASA scientific and technical information system in January 1974

Exploration of neuronal ensembles responsible for sleep and body temperature regulation

Sleep is a behaviour we experience every day but the fundamental function(s) and the neuronal circuitry underlying it remain mystery. Previous study from our laboratory suggests the lateral preoptic (LPO) area of the hypothalamus plays an important role in recovery sleep (RS) after sleep deprivation (SD) as well as 2-adrenergic agonist (dexmedetomidine)-induced sedation and hypothermia. Preliminary data of whole-brain mapping of the neuronal activity of 5-hr SD mice and 2- hr RS (followed 5-hr SD) mice by cFos expression confirmed that the LPO shows higher neuronal activity in RS mice compared to SD mice. Cell-type specific ablation of galaninergic neurons in the LPO abolished sleep homeostasis in mice, in terms of the amount of RS as well as the increased slow wave activity (SWA) of RS after SD which is a hallmark of sleep homeostasis. In addition, mice with ablation of LPOGal neurons have a permanent elevation in their body temperature compared to control mice. LPOGal neurons are also involved in mediating dexmedetomidine (DEX)-induced sedation and hypothermia. Mice without LPOGal neurons have reduced effects: administration of DEX cannot induce high-power oscillations or sustained hypothermia. Together, LPOGal neurons unite sleep homeostasis and 2-adrenergic sedation. Preliminary whole-brain cFos mapping also revealed a few other potential brain regions that might be involved in sleep/wake regulation, including the ventral tegmental area (VTA). Chemogenetic activation and inactivation increase the neuronal activity of VTAVglut2 and VTAVgat neurons, respectively, and both increase wakefulness. VTAVglut2/Nos1 neurons promote wakefulness by sending excitatory projections to both the lateral hypothalamus (LH) and nucleus accumbens (NAc), whereas the wake-inhibiting effect of VTAVgat neurons is achieved by sending inhibitory projections to local VTAVglut2 and VTADA neurons as well as to the orexin neurons in the LH, implying the significance of the VTA in sleep/wake regulation.Open Acces

Brain stimulation techniques as novel treatment options for insomnia: A systematic review.

Despite the success of cognitive behavioural therapy for insomnia and recent advances in pharmacotherapy, many patients with insomnia do not sufficiently respond to available treatments. This systematic review aims to present the state of science regarding the use of brain stimulation approaches in treating insomnia. To this end, we searched MEDLINE, Embase and PsycINFO from inception to 24 March 2023. We evaluated studies that compared conditions of active stimulation with a control condition or group. Outcome measures included standardized insomnia questionnaires and/or polysomnography in adults with a clinical diagnosis of insomnia. Our search identified 17 controlled trials that met inclusion criteria, and assessed a total of 967 participants using repetitive transcranial magnetic stimulation, transcranial electric stimulation, transcutaneous auricular vagus nerve stimulation or forehead cooling. No trials using other techniques such as deep brain stimulation, vestibular stimulation or auditory stimulation met the inclusion criteria. While several studies report improvements of subjective and objective sleep parameters for different repetitive transcranial magnetic stimulation and transcranial electric stimulation protocols, important methodological limitations and risk of bias limit their interpretability. A forehead cooling study found no significant group differences in the primary endpoints, but better sleep initiation in the active condition. Two transcutaneous auricular vagus nerve stimulation trials found no superiority of active stimulation for most outcome measures. Although modulating sleep through brain stimulation appears feasible, gaps in the prevailing models of sleep physiology and insomnia pathophysiology remain to be filled. Optimized stimulation protocols and proof of superiority over reliable sham conditions are indispensable before brain stimulation becomes a viable treatment option for insomnia

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 182, July 1978

This bibliography lists 165 reports, articles, and other documents introduced into the NASA scientific and technical information system in June 1978

Aerospace Medicine and Biology. A continuing bibliography with indexes

This bibliography lists 244 reports, articles, and other documents introduced into the NASA scientific and technical information system in February 1981. Aerospace medicine and aerobiology topics are included. Listings for physiological factors, astronaut performance, control theory, artificial intelligence, and cybernetics are included

Galanin neurons unite sleep homeostasis and α2-adrenergic sedation

Our urge to sleep increases with time spent awake, until sleep becomes inescapable. The sleep following sleep deprivation is longer and deeper, with an increased power of delta (0.5 - 4 Hz) oscillations, a phenomenon termed sleep homeostasis [1-4]. Although widely-expressed genes regulate sleep homeostasis [1, 4-10], and the process is tracked by somnogens and phosphorylation [1, 3, 7, 11-14], at the circuit level sleep homeostasis has remained mysterious. Previously we found that sedation induced with 2 adrenergic agonists (e.g. dexmedetomidine) and sleep homeostasis both depend on the preoptic (PO) hypothalamus [15, 16]. Dexmedetomidine, increasingly used for long-term sedation in intensive care units [17], induces a NREM-like sleep but with undesirable hypothermia [18, 19]. Within the PO, various neuronal subtypes (e.g. GABA/galanin and glutamate/NOS1) induce NREM sleep [20-22] and concomitant body cooling [21, 22]. This could be because NREM sleep’s restorative effects depend on lower body temperature [23, 24]. Here, we show that mice with lesioned PO galanin neurons have reduced sleep homeostasis: in the recovery sleep following sleep deprivation, there is a diminished increase in delta power, and the mice catch up little on lost sleep. Furthermore, dexmedetomidine cannot induce high-power delta oscillations or sustained hypothermia. Some hours after dexmedetomidine administration to wild-type mice there is a rebound in delta power when they enter normal NREM sleep, reminiscent of emergence from torpor. This delta rebound is reduced in mice lacking PO galanin neurons. Thus, sleep homeostasis and dexmedetomidine-induced sedation require PO galanin neurons and likely share common mechanisms

Sleep studies in mice - open and closed loop devices for untethered recording and stimulation

Sleep is an important biological processes that has been studied extensively to date. Research in sleep typically involves mice experiments that use heavy benchtop equipment or basic neural loggers to record ECoG/EMG signals which are then processed offline in workstations. These systems limit the complexity of experiments that can be carried out to only simple open loop recordings, due to either the tethered setup used, which restricts animal movements, or the lack of devices that can offer more advanced features without compromising its portability. With rising popularity in exploring more physiological features that can affect sleep, such as temperature, whose importance has been highlighted in several papers [1][2][3] and advances in optogenetic stimulation, allowing high temporal and spatial neural control, there is now an unprecedented demand for experimental setups using new closed loop paradigms. To address this, this thesis presents compact and lightweight neural logging devices that are not only capable of measuring ECoG and EMG signals for core sleep analysis but also capable of taking high resolution temperature recordings and delivering optogenetic stimulus with fully adjustable parameters. Together with its embedded on-board automatic sleep stage scoring algorithm, the device will allow researchers for the first time to be able to quickly uncover the role a neural circuit plays in sleep regulation through selective neural stimulation when the animal is under the target sleep vigilance state. Original contributions include: the development of two novel multichannel neural logging devices, one for core sleep analysis and another for closed loop experimentation; the development and implementation of a lightweight, fast and highly accurate automatic on-line sleep stage scoring algorithm; and the development of a custom optogenetic coupler that is compatible with most current optogenetic setups for LED-Optical fibre coupling.Open Acces

Acetylcholine neuromodulation in normal and abnormal learning and memory: vigilance control in waking, sleep, autism, amnesia, and Alzheimer's disease

This article provides a unified mechanistic neural explanation of how learning, recognition, and cognition break down during Alzheimer's disease, medial temporal amnesia, and autism. It also clarifies whey there are often sleep disturbances during these disorders. A key mechanism is how acetylcholine modules vigilance control in cortical layer