ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
The subfornical organ, organum vasculosum of the lamina terminalis and nucleus of the solitary tract are all connected to the median preoptic nucleus. This in turn is connected to the paraventricular and supraoptic nuclei of the hypothalamus, which control vasopressin secretion. The nucleus of the solitary tract and preoptic areas are also connected to the lateral hypothalamus, which appears not to be involved in vasopressin regulation, but is involved in the initiation of drinking (see Clark et al., 1991). Clearly, this neural machinery is capable of responding independently to either osmometric or volumetric thirst, as it often must. It is quite conceivable to have for example, blood loss (due to wounding) without there being loss of fluid from the intracellular compartments. It is however also the case that both osmometric and volumetric thirst occur together (as happens when water is lost from the skin by evaporation). Brain processes involved in drinking—which are still not completely understood—are able to deal effectively with these various contingencies.
The neurobiology of sleep
Philip N. Murphy in The Routledge International Handbook of Psychobiology, 2018
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
Clete A. Kushida in Sleep Deprivation, 2004
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.
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.
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.
Fezolinetant in the treatment of vasomotor symptoms associated with menopause
Published in Expert Opinion on Investigational Drugs, 2021
Herman Depypere, Christopher Lademacher, Emad Siddiqui, Graeme L Fraser
This mechanistic explanation for the basis of VMS is derived from various observations in both preclinical and ex vivo studies. Ovariectomy is known to increase tail skin temperature in rats, and this phenomenon is reversed by estradiol treatment [47,48], consistent with the clinical sequelae of menopausal hot flashes [49]. Rance and coworkers recognized hypertrophy in NKB-expressing neurons in the hypothalamic infundibular nucleus of postmenopausal women [50,51], and the corresponding neural network in ovariectomized rats [52]. They further demonstrated that these NKB-expressing KNDy neurons were critical to estrogen modulation of body temperature and the observation of cutaneous vasodilation in ovariectomized rats [46]. More recent work has demonstrated that KNDy neurons project to additional NK3R-expressing neurons in the median preoptic nucleus (MnPO) [53], the site for thermoregulatory control. These findings have culminated in the recognition of this NK3R-sensitive neural circuit as key to the flushing response which arises from a shift in the balance point for core body temperature [46,54], thereby activating heat dissipation effectors [55]. This mechanistic explanation, based on preclinical research, appears to translate well to the clinical setting based on various reports implicating NKB/NK3R signaling in VMS [45,56,57]. Activation of heat dissipation effectors manifests in the clinical symptoms of sweating and cutaneous vasodilation, experienced as hot flashes (Figure 1).
Related Knowledge Centers
- Amygdala
- Limbic System
- Nervous System
- Thermoregulation
- Hippocampus
- Preoptic Area
- Hypothalamus
- Thalamus
- Homeostasis
- NON-Rapid Eye Movement Sleep