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Hypothalamic Neuronal Circuits Are Modulated by Insulin and Impact Metabolism 1
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Tadeu de Oliveira Diz, Sabela Casado, Rubén Nogueiras, Sulay Tovar
The dorsomedial hypothalamic nucleus (DMH) is a brain structure adjacent to the third ventricle, which is located caudal and ventral to the paraventricular nucleus of the hypothalamus (PVN). Its lateral portion is adjacent to both the fornix and the lateral hypothalamic area. The DMH is subdivided into two distinct portions: a diffuse and a compact zone. It contains a high level of NPY terminals and α-MSH terminals originating from the ARC (58). The DMH also contains MCRs in which α-MSH acts generating an anorexigenic response (51). NPY is also expressed by neurons within the DMH. The function of NPY in this nucleus has yet to be fully determined but we know that NPY overexpression in the DMH induces obesity and overeating, whereas NPY downregulation in DMH ameliorates hyperphagia and obesity and delays high fat diet-induced obesity (58, 59) it also improves insulin sensitivity and glucose tolerance, prevented diet-induced hyperglycaemia and hyperinsulinemia (60).
Distribution and Characteristics of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The dorsomedial hypothalamic nucleus (DMH) is located above the ventromedial nucleus and below the caudal part of the PVN. It receives information from neurons and hormones involved in feeding regulation, body weight and energy consumption, and it passes this information on to brain regions involved in sleep and wakefulness regulation, body temperature and corticosteroid secretion. Lesions in the DMH neurons in rats prevent food entrainment of wakefulness, locomotor activity, and core body temperature, verifying its role in oscillation between feeding and the circadian rhythm. Such lesions also caused a weakened level of response to feeding stimulation by insulin.
Adrenal-dependent and -independent stress-induced Per1 mRNA in hypothalamic paraventricular nucleus and prefrontal cortex of male and female rats
Published in Stress, 2018
Lauren E. Chun, Jenny Christensen, Elizabeth R. Woodruff, Sarah J. Morton, Laura R. Hinds, Robert L. Spencer
The SCN has relatively limited neural projections (Watts, Swanson, & Sanchez-Watts, 1987), and thus may communicate with extra-SCN clocks through the release of glucocorticoid hormones (corticosterone in the rat). Corticosterone is released upon activation of the hypothalamic-pituitary-adrenal (HPA) axis. Neural input to the hypothalamic paraventricular nucleus (PVN) initiates a neuroendocrine cascade that ultimately drives the release of corticosterone. The HPA axis receives both stress-related (Ulrich-Lai & Herman, 2009) and circadian-related neural input (Dickmeis, 2009). Corticosterone has an SCN-dependent diurnal rhythm (Kalsbeek, Liu, et al., 2012) that is due to SCN neural input to both the PVN and adrenal elements of the HPA axis. The SCN projects both directly and indirectly (via the subparaventricular zone of the PVN and via the dorsomedial hypothalamic nucleus) to corticotropin-releasing hormone neurons in the PVN (Buijs, Markman, Nunes-Cardoso, Hou, & Shinn, 1993; Kalsbeek, van der Spek, et al., 2012; Watts et al., 1987). The SCN also regulates the circadian release of corticosterone by modulating adrenal sensitivity to ACTH via the splanchnic nerve (Buijs et al., 2003; Ulrich-Lai, Arnhold, & Engeland, 2006).
Pre-exercise exposure to the treadmill setup changes the cardiovascular and thermoregulatory responses induced by subsequent treadmill running in rats
Published in Temperature, 2018
Ana C. Kunstetter, Nicolas H. S. Barbosa, Michele M. Moraes, Valéria A. Pinto, Danusa D. Soares, Washington Pires, Samuel P. Wanner
The physiological responses to pre-exercise treadmill exposure observed in our study likely reflect a stress-related response caused by handling and transfer to an environment that induces anxiety, as the rats avoid the electrical grid and remain alert, expecting the treadmill to be turned on. These stress-related responses are somewhat similar to those promoted by psychological stress paradigms, such as cage-switch or air-jet stress. Previous studies demonstrated that MAP and HR rapidly increased during the first minutes of cage-switch stress,37-39 while TCORE increased at a slower rate over 30 min of exposure to this type of stress.38 In addition, Kiyatkin et al.40 observed that aortic and brain temperatures, two different indices of TCORE, increased by approximately 1.8°C in response to transfer from a home cage to a test cage, with this stress-induced hyperthermia lasting for approximately 90 min. Additional evidence suggesting that these physiological changes are stress-related responses is the fact that dorsomedial hypothalamic nucleus lesions attenuate the increase in TCORE induced by placing an animal on a treadmill (Wanner et al., unpublished observations); the same lesions also attenuated hyperthermia following handling and injection of intraperitoneal saline in rats.41 Of note, monosynaptic excitatory neurotransmission from the dorsomedial hypothalamus to sympathetic premotor neurons in the rostral medullary raphe region drives brown adipose tissue thermogenesis and tachycardia, leading to the development of psychological stress hyperthermia.42
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
The brain areas which mainly exchange information with the SCN and function as effectors for their circadian rhythmicity are the hypothalamic paraventricular nucleus (PVN), the dorsomedial hypothalamic nucleus (DMH) and median preoptic area (MnPO). These nuclei integrate the temporal information with internal cues to regulate body temperature, stress response and endocrine secretion, metabolism and sleep, among other homeostatic and behavioral functions (Buijs et al. 2003; Chou et al. 2003; Gooley et al. 2006; Guzmán-Ruiz et al. 2015; Neumann et al. 2019; Oster 2020; Saper and Machado 2020).