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Control of the Upper Airway during Sleep
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
The second REM sleep-related group comprises the cells located in the posterior lateral hypothalamus that synthesize melanin-concentrating hormone (MCH) (156). MCH cells have extensive axonal projections that extend to the pontomedullary reticular formation but their specific targets need studies (157). Although MCH is their unique neurochemical marker, they also use GABA as their transmitter (158). Thus, their enhanced activity during REM sleep would inhibit their postsynaptic targets. Another GABAergic group of REM sleep-active cells is located in a small subregion of the anterior hypothalamus called the extended ventrolateral preoptic nucleus (eVLPO). These cells facilitate the generation of REM sleep through their extensive ascending and descending projections (159).
Consciousness, Sleep and Hypnosis, Meditation, and Psychoactive Drugs
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
The suprachiasmatic nucleus of the hypothalamus is the circadian rhythm generator controlling the sleep–wake cycle, presumably by modulating the sleep–wake regulatory system, including the ventrolateral preoptic nucleus (VLPO) of the hypothalamus. The VLPO sends projections to the histaminergic tuberomamillary nucleus (TMN), the serotonergic dorsal and median raphe nucleus, and the noradrenergic locus ceruleus. It also sends axons that terminate within the cholinergic basal forebrain, the pedunculopontine thalamic (PPT) nucleus and the lateral dorsal thalamic (LDT) nucleus. The VLPO projections to these areas are inhibitory in nature as they are γ-aminobutyric acid-ergic (GABAergic) and galaninergic. The VLPO, via its inhibition of the major arousal mechanisms, functions as a “sleep switch,” promoting sleep. Its reciprocal relationship with the major arousal areas helps it to function as one half of a “flip-flop” circuit, which prevents intermediate states of sleep and wakefulness (Saper, Chou, & Scammell, 2001; Saper, Lu, Chou, & Gooley, 2005).
Normal Sleep
Published in Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam, Clinical Atlas of Polysomnography, 2018
Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam
The homeostatic (also known as “S”) process makes us feel sleepy depending upon the duration of wakefulness. The longer the period of wakefulness, the higher the sleep pressure; in other words, higher are the chances to fall asleep. That is the reason why a person who is awake for a long time falls asleep even during the day. Moreover, this process regulates the proportion of deep sleep (N3 sleep) - the longer the period of wakefulness, the higher the proportion of deep sleep. The homeostatic process is dependent upon two major areas of the brain that are located close to the hypothalamus. The first is the sleep-promoting area - the ventrolateral preoptic nucleus (VLPO), which sends inhibitory signals through the GABAergic neurons to the wake-promoting area of the brain. Wakefulness is dependent upon the monoaminergic nuclei of the brain that are the part of the reticular activating system (RAS). Monoaminergic nuclei include serotonergic neurons (located in dorsal and medial raphe nuclei), noradrenergic neurons (locus coeruleus), histaminergic neurons (tuber- omammillary nucleus) and cholinergic neurons (located in pedunculopontine (PPT), laterodorsal tegmental (LDT) nuclei, and basal forebrain nuclei). In addition, there are glutaminergic neurons that are diffusely distributed throughout the RAS. When the VLPO sends GABArgic signals to these neurons, sleep ensues. The activity of both wake-promoting and sleep-promoting areas is modulated through another group of neurons, the hypocretin neurons that are present in the lateral and posterior hypothalamus. Under normal conditions, the hypocretin neurons modulate the activity of the other two areas of the brain in such a manner that only one state of consciousness, that is, wakefulness or sleep prevails (Figure 1.1). Damage to the hypocretin neurons leads to a condition known as narcolepsy. In this condition, a person is not able to maintain either states and experiences bouts of sleepiness during wakefulness.
Sleep-promoting activity of lotus (Nelumbo nucifera) rhizome water extract via GABAA receptors
Published in Pharmaceutical Biology, 2022
Yejin Ahn, Singeun Kim, Chunwoong Park, Jung Eun Kim, Hyung Joo Suh, Kyungae Jo
Currently, the understanding on how stress affects sleep is obscure, but is suspected to be closely related to sleep and the activity of the hypothalamic-pituitary-adrenal (HPA) axis. In the early stages of sleep, slow wave sleep is dominant, and the activity of the HPA axis is the lowest and continuously suppressed. Conversely, in the second half of sleep, REM sleep dominates and the activity of HPA secretion increases, approaching a daily maximum immediately after waking up. The ventrolateral preoptic nucleus (VLPO) located in the hypothalamus acts as a switch to initiate sleep. Activated VLPO neurons secrete inhibitory neurotransmitters, such as GABA, to inhibit the areas responsible for arousal and induce sleep (Saper et al. 2005). GABAs are activated during sleep and inhibit monoamine and histamine-secreting regions to prevent waking. The thalamic reticular nucleus also contains GABA as a neurotransmitter and generates sleep spindles (Mignot et al. 2002).
Temporal dysregulation of hypothalamic integrative and metabolic nuclei in rats fed during the rest phase
Published in Chronobiology International, 2022
Oscar D. Ramirez-Plascencia, Nadia Saderi, Skarleth Cárdenas Romero, Omar Flores Sandoval, Adrián Báez-Ruiz, Herick Martínez Barajas, Roberto Salgado-Delgado
An extensive amount of evidence shows that conflicts between the rhythms ruled by the SCN and alterations of physiology and behavior could be harmful to any organism (Roenneberg and Merrow 2016). In particular, food intake during the rest period is linked to the disruption of daily patterns of body temperature, locomotor activity and serum levels of triglycerides, glucose, corticosteroid, leptin and ghrelin (Mukherji et al. 2015; Salgado-Delgado et al. 2010); alterations in the expression of peripheral clock and metabolism-related genes (Mukherji et al. 2015; Opperhuizen et al. 2016; Salgado-Delgado et al. 2013); increased fat mass accumulation, reduced energy expenditure and glucose intolerance (Bray et al. 2013; Opperhuizen et al. 2016; Salgado-Delgado et al. 2010); alterations in the daily activity of hypothalamic nuclei involved in metabolic and sleep/wake regulation, such as the arcuate nucleus, perifornical area, lateral hypothalamic and the ventrolateral preoptic nuclei (Ramirez-Plascencia et al. 2017; Wang et al. 2017).
Sedative drugs used for mechanically ventilated patients in intensive care units: a systematic review and network meta-analysis
Published in Current Medical Research and Opinion, 2019
Hongliang Wang, Changsong Wang, Yue Wang, Hongshuang Tong, Yue Feng, Ming Li, Liu Jia, Kaijiang Yu
The development of delirium may be caused by many factors, such as pre-existing Alzheimer’s disease, hypertension, inflammation, organ failure, age, severity of illness, a history of alcoholism or the severity of the disease at hospital admission48,58. Sedatives and analgesics also have effects on delirium33,36,39,47. In our study, we concluded that benzodiazepine administration causes an increased risk of delirium compared to α2 adrenoreceptor agonists. Benzodiazepine drugs have a high affinity for GABAA receptors, and their activation may alter the levels of numerous neurotransmitters considered deliriogenic47. In addition to altering neurotransmitter concentrations, benzodiazepine drugs impair the quality of sleep via slow-wave sleep suppression, which thus contributes to delirium47. Pandharipande et al. suggested that in contrast to benzodiazepine drugs, which act directly at the level of the tuberomammillary nucleus and the ventrolateral preoptic nucleus, dexmedetomidine (an α2 adrenoreceptor agonist) acts at the level of the locus coeruleus. Dexmedetomidine has a different neurotransmitter profile and preserves slow-wave (deep, non-rapid eye movement) sleep48. Furthermore, the anti-inflammatory effects of dexmedetomidine may contribute to a reduction in the risk of delirium48.