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Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
Descending inhibitory system: sleep-promoting (Figure 28.12): Inhibitory projections arise from the VLPO area and associated neuronal groups, such as the median preoptic nucleus, to initiate and maintain sleep.Inhibitory projections synapse on multiple nuclei of the reticular activating system.Neurotransmitters are gamma-aminobutyric acid (GABA) and galanin.
The neurobiology of sleep
Published in Philip N. Murphy, The Routledge International Handbook of Psychobiology, 2018
Roman Rutka, Sonia Pellissier, Pascal Hot
As described above, wakefulness is made possible by the activity of specific brain structures. This activity must therefore be inhibited to allow sleep onset, and a number of mechanisms may be involved. In the anterior part of the hypothalamus, several groups of neurons are selectively active during sleep. Some of these groups are clustered in the median preoptic nucleus (MnPO), which is thought to have an important role in triggering sleep onset. Moreover, an estimated 40% of the MnPO’s neurons use the well-known inhibitory neurotransmitter gamma aminobutyric acid (GABA) (Gong et al., 2004; Gvilia, Angara, McGinty, & Szymusiak, 2005). These neurons are connected to several wake-promoting regions, including the locus coeruleus and the dorsal raphe nucleus; the results of animal studies have confirmed that the MnPO’s neurons can inhibit these structures (Suntsova et al., 2007). These data support the hypothesis whereby the MnPO is responsible for sleep onset (Suntsova, Szymusiak, Alam, Guzman-Marin, & McGinty, 2002). Even though it has been proposed that the MnPO’s only hypnic function is to trigger sleep onset, Benedetto and colleagues found that pharmacological inhibition of this structure not only prevents NREM sleep but also inhibits REM sleep and promotes awakening in sleeping cats (Benedetto, Chase, & Torterolo, 2012). Therefore, it is currently thought that the MnPO promotes both sleep onset and sleep maintenance.
Recovery from Sleep Deprivation
Published in Clete A. Kushida, Sleep Deprivation, 2004
Thomas S. Kilduff, Clete A. Kushida, Akira Terao
Although the homeostatic drive to sleep accrues primarily during wake-fulness, its physiological manifestation, Process S, is measured only during the ensuing sleep period. Since SWA can be directly measured during RS, determination of gene expression during RS is an attractive paradigm because mRNA or protein levels can be directly correlated with SWA levels. Although this approach is yet to be extensively used in molecular studies of sleep, it has led to the identification of the ventrolateral preoptic area (VLPO) as a sleep-active region through correlation of Fos expression with increased SWA during NREM sleep (63). Fos expression in the VLPO has been positively correlated with the preceding amount of both naturally occurring (63) and pharmacologically induced sleep (64). A positive correlation with sleep induced by warming has also been found in the median preoptic nucleus (65). These and other studies indicate that gene expression varies with behavioral state in a brain region-specific manner.
Circadian and ultradian rhythms in normal mice and in a mouse model of Huntington’s disease
Published in Chronobiology International, 2022
Christopher G. Griffis, Janki Mistry, Kendall Islam, Tamara Cutler, Christopher S. Colwell, Alan Garfinkel
The control of CBT is mediated by a hierarchically organized set of hypothalamic structures with the preoptic area and the median preoptic nucleus at the top of it (Saper and Lowell 2014). Circadian rhythms in CBT are independent of locomotor activity but dependent upon an intact SCN (Ruby et al. 2002; Scheer et al. 2005; Stephan and Nunez 1977). Pre-symptomatic HD patients were reported to have an elevated daytime CBT (Schultz et al. 2021), but rhythms were not measured. Therefore, future studies will need to determine whether these ultradian rhythms that are so prominent in the mouse models are also present in the patient population. New technologies allow CBT to be continuously measured through wireless capsules, and perhaps even wearable devices, which should facilitate measurements in patient populations.
Estradiol alters body temperature regulation in the female mouse
Published in Temperature, 2018
Sally J. Krajewski-Hall, Elise M. Blackmore, Jessi R. McMinn, Naomi E. Rance
We have previously described a central effect of senktide on body temperature in the rat via NK3 receptor-expressing neurons in the median preoptic nucleus.7,10 The median preoptic nucleus is part of the heat dissipation pathway that receives information from warm-sensitive, cutaneous thermoreceptors.59 In turn, projections from the median preoptic nucleus reduce TCORE via cutaneous vasodilation and activation of other heat dissipation effectors.59 Microinfusion of senktide directly into the median preoptic nucleus of the rat selectively activates fos within the median preoptic nucleus and results in hypothermia.7 These effects are duplicated by subcutaneous injections of senktide.10 If NK3 receptor-expressing neurons in the median preoptic nucleus are ablated, subcutaneous senktide injections do not result in hypothermia or fos activation in the median preoptic nucleus.10 Thus, NK3 receptor-expressing neurons in the median preoptic nucleus are required (and sufficient) for senktide to induce hypothermia in the rat.
Role of the median preoptic nucleus in the autonomic response to heat-exposure*
Published in Temperature, 2018
Stephen B.G. Abbott, Clifford B. Saper
The preoptic area (POA) is a critical brain region for the regulation of body temperature in mammals. Neurons in the POA are believed to integrate information concerning environmental temperature, endocrine and metabolic status, as well as inflammatory and environmental threats, to optimize body temperature through adaptive behaviors, thermogenesis and active and passive heat-loss mechanisms. According to a prevalent model [1], body temperature homeostasis during heat-exposure is proposed to be mediated by warm-activated glutamatergic neurons in the median preoptic nucleus (MnPO), which then act on local GABAergic neurons in the medial preoptic area that inhibit heat production by brown adipose tissue (BAT) and shivering and promote passive heat-loss by increasing cutaneous blood flow.