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Energy balance and its regulation
Published in Geoffrey P. Webb, Nutrition, 2019
A spontaneously active feeding centre that initiates food-seeking and eating behaviour was envisaged as being located in the lateral hypothalamus. Its destruction by lateral hypothalamic lesions results in a cessation of eating behaviour. This feeding centre was said to be periodically inhibited by a satiety centre located in the ventromedial region of the hypothalamus. This satiety centre would become active in response to certain satiety signals, which strengthen after feeding; it would then inhibit the feeding centre and produce satiation. As time after feeding elapses, so one would envisage these satiety signals dying away, and the satiety centre would become quiescent, allowing the feeding centre to become active again and producing hunger. One could envisage longer-term signals, like the amount of stored body fat, increasing the activity of this satiety centre. Destruction of this satiety centre would reduce satiation and result in excessive food consumption and obesity. The hypothalamus is thus envisaged as acting like a meter or “appestat” that adjusts the feeding drive in response to a variety of physiological signals that reflect the short- and long-term energy status of the body – energy intake is thus matched to output and energy balance is maintained.
Hypothalmic-Pituitary Regulation and Aging
Published in Richard C. Adelman, George S. Roth, Endocrine and Neuroendocrine Mechanisms of Aging, 2017
Arthur V. Everitt, Jennifer Wyndham
Small bilateral lesions in the lateral hypothalamic feeding center depress food intake by about 20%, thereby leading to a slower rate of body growth.67 The effects of such lesions on aging have not been investigated. One criticism of this technique is a possible lack of specificity since the lateral hypothalamus affects thirst and perhaps other functions.
Histamine as Neurotransmitter
Published in Divya Vohora, The Third Histamine Receptor, 2008
Oliver Selbach, Helmut L. Haas
Neurons in the ventromedial hypothalamus (VMH) contain the liberating or inhibiting hormones for hormone release from the hypophysis, the peptides growth hormone-releasing hormone (GHRH), prolactin-releasing hormone (PRH), TRH, CRH, gonadotrophin-releasing hormone (GnRH), and dopamine (prolactin-inhibiting hormone, PIH). The histaminergic neurons densely innervate these regions and participate in the regulation of pituitary hormone secretion through both H1 and H2R [277]. The histamine-induced secretion of ACTH, beta-endorphin, and prolactin seems to be mediated through activation of hypothalamic ADH, oxytocin, and CRH neurons. Stress-induced corticosterone release is modulated by histamine [277,278]. Release of the anabolic hormones, growth harmone (GH) and thyroid-stimulating harmone (TSH), is inhibited through exogenous (icv) and endogenous histamine, presumably through an action on TRH- and GHRH-containing neurons at the hypothalamic level [279]. Early ionophoretic studies reported H1R-mediated excitation and H2R-mediated depression of firing [280,281]. An H1R-mediated excitation was found in arcuate nucleus neurons [282]. The perifornical area and lateral hypothalamus contains the orexin/hypocretin neurons that activate and orchestrate the aminergic wake-promoting nuclei. Although there is a strong mutual innervation between this nucleus and the TMN, an electrophysiological action has only been seen in one direction so far: hypocretins excite histaminergic neurons [95], but histamine seems to be ineffective on hypocretin neurons in vitro [283].
Nutrient infusion evoked magnetic resonance imaging signal in the human hypothalamus
Published in Nutritional Neuroscience, 2022
Yuko Nakamura, Mariko Takahashi, Yukiko Inoue, Shintaro Yanagimoto, Kazuo Okanoya, Shinsuke Koike
Even though there was no significant difference in ratings for hunger across fMRI sessions, only hypothalamic responses to saline showed a significant negative association with ratings for hunger. Although the lateral hypothalamus has been reported to contribute to food intake [35], recent studies have shown that the lateral hypothalamus may be connected to other hypothalamic nuclei and other CNS regions [15]. In addition, lateral hypothalamus activation was associated with both hunger and satiety in humans [36]. These previous reports suggest that the lateral hypothalamus may mediate hunger as well as fullness to serve as one of key centers in the regulation of eating behavior. Given that only hypothalamic responses to saline showed a significant negative association with ratings for hunger in this study, decreased hypothalamic responses may be linked to hunger sensation and increased lateral hypothalamic responses in response to nutrient infusion could attenuate hunger sensations, although there was no significant association between hypothalamic responses and internal state ratings in nutrient conditions.
Twenty-four-hour variation of vestibular function in young and elderly adults
Published in Chronobiology International, 2021
Tristan Martin, Amira Zouabi, Florane Pasquier, Pierre Denise, Antoine Gauthier, Gaëlle Quarck
The second hypothesis is vestibular function exhibits temporal variation, perhaps mediated by the body clock like other circadian physiological functions. This would not be surprising, since vestibular nuclei are indirectly connected to the suprachiasmatic nuclei via the intergeniculate leaflet (Horowitz et al. 2004) as well as the visual pathways. A pathway between vestibular nuclei and posterior hypothalamus has been shown, the latter playing an important role in biological rhythmicity (Cavdar et al. 2001). Reciprocal connections between vestibular nuclei and orexin neurons of the lateral hypothalamus have been demonstrated; orexin neurons play a role in the sleep-wake cycle (Horowitz et al. 2005). We have previously postulated that these pathways can convey vestibular information to the biological clock to help circadian rhythm synchronization, since both vestibular stimulation (2 G exposure) and loss drastically modify circadian rhythms (Fuller et al. 2002; Martin et al. 2015, 2016; Murakami et al. 2002). It is thus plausible the biological clock can reciprocally influence vestibular responses through hypothalamic-vestibular neural pathways, generating a circadian rhythm of VOR responses.
Orexin/hypocretin receptor, Orx1, gene variants are associated with major depressive disorder
Published in International Journal of Psychiatry in Clinical Practice, 2019
Mujgan Cengiz, Vilson Karaj, Nese Kocabasoğlu, Gokcen Gozubatik-Celik, Ahmet Dirican, Burcu Bayoglu
Orexin neuropeptides have significant roles in circadian clock since they involve in sleep-wake transition in humans (Sakurai, Mieda, & Tsujino, 2010). Circadian clocks in glucocorticoids, dopamine, orexin/melanin-concentrating hormone (MCH) systems control key aspects of metabolism and brain functions including energy expenditure and arousal (Barandas, Landgraf, McCarthy, & Welsh, 2015). There are also other polypeptides expressed in lateral hypothalamus other than orexins including melanin-concentrating hormone (MCH) (Bittencourt et al., 1992). A disruption in MCH regulation was also reported in MDD pathogenesis (Chung, Parks, Lee, & Civelli, 2011; Roy, David, Cueva, & Giorgetti, 2007). Orexin was shown to have a tight relationship with MCH having a role in sleep/wake cycle (Schmidt et al., 2013). Impaired sleep/wakefulness regulation is frequently found in MDD such as extended sleep latency, diminished REM latency, elevated total REM sleep, decreased total slow-wave sleep (Palagini, Baglioni, Ciapparelli, Gemignani, & Riemann, 2013). MDD patients frequently have sleep disorders and also display symptoms including disrupted regulation of wakefulness accompanied by hyperarousal and agitation. Besides, they have symptoms like difficulties to falling asleep and preserving sleep continuity (Schmidt et al., 2011).