Acute lesions of the ventromedial hypothalamus reduce sympathetic activation and thermogenic changes induced by PGE1
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Cited by (21)
Traveling from the hypothalamus to the adipose tissue: The thermogenic pathway
2017, Redox BiologyCitation Excerpt :During infections, prostaglandins (PG) are released in the vasculature and peripheral tissues and upon arrival to the POA trigger activation of the BAT thermogenic program [27–29]. Specifically, POA contains PG receptors subtype EP3, which are connected to the dorsomedial nucleus of the hypothalamus (DMH), as well as the rostral raphe pallidus (rRPA) in the brainstem that control thermogenesis in BAT to induce fever through a mechanism that involve cAMP [27–30]. A population of the POA neurons expressing EP3 subtype of PGE receptor is mainly GABAergic and projects to DMH and the rRPa antagonizing some inhibitory fibers to induce fever [30].
Neuromodulation for Eating Disorders. Obesity and Anorexia.
2014, Neurosurgery Clinics of North AmericaCitation Excerpt :The VMH acts as a “satiety center,” which is the set point for regulation of caloric intake, whereas the LHA acts as a “feeding center.”32 Thus, activation of the VMH or a lesion of the LHA induces primary increases in metabolism rates that precede and parallel the period of food-intake inhibition.26,33,34 In other words, the modulation of these neural structures results in a tendency toward weight loss by way of a double influence on both sides of the energy balance.
The Hepatic Vagus Nerve Attenuates Fas-Induced Apoptosis in the Mouse Liver via α7 Nicotinic Acetylcholine Receptor
2008, GastroenterologyCitation Excerpt :At present, we cannot fully explain the reason for this discrepancy between our present results and theirs; however, this experiment was performed without any liver stimulation, and the increasing apoptotic results were evaluated starting from the very early state of 24 hours after lesioning of the ventromedial hypothalamus. In addition, this ventromedial hypothalamic lesioning has also been shown to reduce the sympathetic nervous activation,25,26 which thus indicates that the acute stressful situation following brain surgery that was noted in the study of Kiba et al is quite different from the physiologic situation noted in our study, 1 week after hepatic vagotomy. Some recent studies have reported that the anti-inflammatory effect of the efferent vagus nerve is mediated through the α7 nicotinic AChRs.11
Intracerebroventricular injection of prostaglandin E<inf>1</inf> changes concentrations of biogenic amines in the posterior hypothalamus of the rat
2000, Brain ResearchCitation Excerpt :Indeed, the turnover rate of catecholamines in the PH is associated with an increase in the activity of the sympathetic nervous system in rats with hypertension [3,37], while lead exposure is associated with changes in the level of catecholamines in the PH [16]. Since an icv injection of PGE1[17,21] or PGE2[11] induces an increase in sympathetic activity, while pre-treatment with an icv administration of the catecholamine-depleting agent, 6-hydroxydopamine, abolishes the febrile responses [26], the aim of this study was to evaluate the changes in adrenaline, noradrenaline and dopamine levels in the PH during the hyperthermia induced by PGE1. We used male Sprague–Dawley rats (n=12), weighing 280–320 g.