Dorsomedial Nucleus of the Thalamus

Keyword(s):  
2012 ◽  
Vol 303 (7) ◽  
pp. E853-E864 ◽  
Author(s):  
Xinfu Guan ◽  
Xuemei Shi ◽  
Xiaojie Li ◽  
Benny Chang ◽  
Yi Wang ◽  
...  

Glucagon-like peptides (GLP-1/2) are cosecreted from endocrine L cells in the gut and preproglucagonergic neurons in the brain. Peripheral GLP-2 action is essential for maintaining intestinal homeostasis, improving absorption efficiency and blood flow, promoting immune defense, and producing efficacy in treatment of gastrointestinal diseases. However, it is unknown if CNS GLP-2 plays a physiological role in the control of energy homeostasis. Since GLP-1/2 are cotranslated from preproglucagongene and coproduced by prohormone convertase-1, it is challenging to knockout GLP-2 only. Instead, our laboratory has generated a Glp2r-floxed mouse line to dissect cell-specific GLP-2 receptor GLP-2R) action in the regulation of energy balance. Our objective was to determine if GLP-2R in the hypothalamus modulates feeding behavior and gastric emptying. We show that Glp2r mRNA and protein are highly expressed in the arcuate nucleus and dorsomedial nucleus of the mouse hypothalamus. Using the Cre-LoxP system, we generated mice that lack Glp2r expression in POMC neurons (KO; mainly in the hypothalamus). The KO mice showed hyperphagic behavior (such as increases in food intake and meal frequency), accelerated gastric emptying (assessed by [13C]octanoic acid breath test), and late-onset obesity, yet there was no decrease in basal metabolic rate. Infusion of GLP-2 (2.5 nmol into the 4th ventricle) suppressed food intake and gastric emptying, while GLP-2-mediated effects were abolished in the melanocortin receptor-4 (MC4R) KO mice. We conclude that Glp2r deletion in POMC neurons enhances feeding behavior and gastric motility, whereas icv GLP-2R activation suppresses food intake and gastric emptying through the MC4R signaling pathway. This study indicates that CNS GLP-2R plays a physiological role in the control of feeding behavior and gastric emptying and that this is mediated probably through the melanocortin system.


1987 ◽  
Vol 66 (4) ◽  
pp. 548-554 ◽  
Author(s):  
Seigo Nagao ◽  
Tsukasa Nishiura ◽  
Hideyuki Kuyama ◽  
Masakazu Suga ◽  
Takenobu Murota

✓ The authors report the results of a study to evaluate the effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure (ICP) after the hypothalamic dorsomedial nucleus and midbrain reticular formation were destroyed. Systemic arterial pressure (BP), ICP, and local cerebral blood volume (CBV) were continuously recorded in 32 cats. To assess the changes in the cerebral vasomotor tonus, the vasomotor index defined by the increase in ICP per unit change in BP was calculated. In 29 of the 32 animals, BP, ICP, and CBV increased simultaneously immediately after stimulation. The increase in ICP was not secondary to the increase in BP, because the vasomotor index during stimulation was significantly higher than the vasomotor index after administration of angiotensin II. The vasomotor index was high during stimulation of the area around the nucleus reticularis parvocellularis. In animals with the spinal cord transected at the C-2 vertebral level, ICP increased without a change in BP. These findings indicate that the areas stimulated in the medullary reticular formation play an important role in decreasing cerebral vasomotor tonus. This effect was not influenced by bilateral superior cervical ganglionectomy, indicating that there is an intrinsic neural pathway that regulates cerebral vasomotor tonus directly. In three animals, marked biphasic or progressive increases in ICP up to 100 mm Hg were evoked by stimulation. The reduction of cerebral vasomotor tonus and concomitant vasopressor response induced by stimulation of the medullary reticular formation may be one of the causes of acute brain swelling.


2021 ◽  
Author(s):  
Thomas Guttuso ◽  
Daniel Sirica ◽  
Duygu Tosun ◽  
Robert Zivadinov ◽  
Ofer Pasternak ◽  
...  

A neural model is presented, based largely on evidence from studies in monkeys, postulating that coded representations of stimuli are stored in the higher-order sensory (i.e. association) areas of the cortex whenever stimulus activation of these areas also triggers a cortico-limbo-thalamo-cortical circuit. This circuit, which could act as either an imprinting or rehearsal mechanism, may actually consist of two parallel circuits, one involving the amygdala and the dorsomedial nucleus of the thalamus, and the other the hippocampus and the anterior nuclei. The stimulus representation stored in cortex by action of these circuits is seen as mediating three different memory processes: recognition, which occurs when the stored representation is reactivated via the original sensory pathway; recall, when it is reactivated via any other pathway; and association, when it activates other stored representations (sensory, affective, spatial, motor) via the outputs of the higher-order sensory areas to the relevant structures.


1986 ◽  
Vol 251 (6) ◽  
pp. R1221-R1227 ◽  
Author(s):  
K. Tokunaga ◽  
M. Fukushima ◽  
J. W. Kemnitz ◽  
G. A. Bray

Lesions in the ventromedial hypothalamus (VMH) uniformly produced obesity, but lesions in the paraventricular nucleus (PVN) produced obesity in only half of the animals. The obesity in the PVN-lesioned animals was related to the extent of PVN damage and was attenuated by concurrent damage to the dorsomedial nucleus. Comparing the PVN-lesioned rats that became obese with the VMH-lesioned rats that showed comparable weight gain, revealed several differences. The nocturnal intake of food in rats eating ad libitum was lower in the VMH-lesioned rats. Glucose concentrations were also lower in the VMH-lesioned rats, whether eating ad libitum or pair fed. Insulin concentrations were higher in the fatter animals fed ad libitum regardless of the location of the lesion. After pair feeding the insulin values were lower in both VMH- and PVN-lesioned rats than in controls. The diurnal excursion of corticosterone was blunted by both hypothalamic lesions in rats fed ad libitum, but after pair feeding there was less distortion of the diurnal rhythm. These data show that the characteristics of obesity produced by PVN lesions differ from those resulting from VMH damage.


Endocrinology ◽  
2000 ◽  
Vol 141 (7) ◽  
pp. 2703-2706 ◽  
Author(s):  
Anders Juréus ◽  
Matthew J. Cunningham ◽  
Molly E. McClain ◽  
Donald K. Clifton ◽  
Robert A. Steiner

Galanin-like peptide (GALP), which was recently isolated from the porcine hypothalamus, shares sequence homology with galanin and binds with high affinity to galanin receptors. To study the distribution and regulation of GALP-expressing cells in the brain, we cloned a 120 base-pair cDNA fragment of rat GALP and produced an antisense riboprobe. In situ hybridization for GALP mRNA was then performed on tissue sections throughout the forebrain of adult ovariectomized female rats. We found GALP mRNA-containing cells in the arcuate nucleus (Arc), caudal dorsomedial nucleus, median eminence and the pituitary. Because GALP mRNA in the Arc appeared to overlap with the known distribution of leptin receptor mRNA, we tested the hypothesis that GALP expression is regulated by leptin. Using in situ hybridization, we compared the number of GALP mRNA-containing cells among groups of rats that were fed ad lib or fasted for 48 h and treated with either leptin or vehicle. Fasting reduced the number of identifiable cells containing GALP mRNA in the Arc, whereas the treatment of fasted animals with leptin produced a 4-fold increase in the number of cells expressing GALP message. The presence of GALP mRNA in the hypothalamus and pituitary and its regulation by leptin suggests that GALP may have important neuroendocrine functions, including the physiological regulation of feeding, metabolism, and reproduction.


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