scholarly journals Influence of the Hypothalamic Arcuate Nucleus on Intraocular Pressure and the Role of Opioid Peptides

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e82315 ◽  
Author(s):  
Ji Jin ◽  
Guo-xu Xu ◽  
Zhi-lan Yuan
Keyword(s):  
Intraocular Pressure ◽  
Opioid Peptides ◽  
Arcuate Nucleus ◽  
Hypothalamic Arcuate Nucleus

scholarly journals Estrogenic-dependent glutamatergic neurotransmission from kisspeptin neurons governs feeding circuits in females

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jian Qiu ◽  
Heidi M Rivera ◽  
Martha A Bosch ◽  
Stephanie L Padilla ◽  
Todd L Stincic ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Arcuate Nucleus ◽  
Neuronal Excitability ◽  
Glutamate Release ◽  
Metabotropic Receptors ◽  
Hypothalamic Arcuate Nucleus ◽  
17Β Estradiol ◽  
Arcuate Neurons ◽  
Feeding Circuits

The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1ARH) neurons are essential for pulsatile release of GnRH and reproduction. Since 17β-estradiol (E2) decreases Kiss1 and Tac2 mRNA expression in Kiss1ARH neurons, the role of Kiss1ARH neurons during E2-driven anorexigenic states and their coordination of POMC and NPY/AgRP feeding circuits have been largely ignored. Presently, we show that E2 augmented the excitability of Kiss1ARH neurons by amplifying Cacna1g, Hcn1 and Hcn2 mRNA expression and T-type calcium and h-currents. E2 increased Slc17a6 mRNA expression and glutamatergic synaptic input to arcuate neurons, which excited POMC and inhibited NPY/AgRP neurons via metabotropic receptors. Deleting Slc17a6 in Kiss1 neurons eliminated glutamate release and led to conditioned place preference for sucrose in E2-treated KO female mice. Therefore, the E2-driven increase in Kiss1 neuronal excitability and glutamate neurotransmission may play a key role in governing the motivational drive for palatable food in females.

scholarly journals Hypothyroidism Compromises Hypothalamic Leptin Signaling in Mice

2013 ◽  
Vol 27 (4) ◽  
pp. 586-597 ◽  
Author(s):  
Claudia Groba ◽  
Steffen Mayerl ◽  
Alies A. van Mullem ◽  
Theo J. Visser ◽  
Veerle M. Darras ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Double Knockout ◽  
Hypothalamic Arcuate Nucleus ◽  
The Central Nervous System ◽  
Leptin Expression ◽  
The Impact

Abstract The impact of thyroid hormone (TH) on metabolism and energy expenditure is well established, but the role of TH in regulating nutritional sensing, particularly in the central nervous system, is only poorly defined. Here, we studied the consequences of hypothyroidism on leptin production as well as leptin sensing in congenital hypothyroid TRH receptor 1 knockout (Trhr1 ko) mice and euthyroid control animals. Hypothyroid mice exhibited decreased circulating leptin levels due to a decrease in fat mass and reduced leptin expression in white adipose tissue. In neurons of the hypothalamic arcuate nucleus, hypothyroid mice showed increased leptin receptor Ob-R expression and decreased suppressor of cytokine signaling 3 transcript levels. In order to monitor putative changes in central leptin sensing, we generated hypothyroid and leptin-deficient animals by crossing hypothyroid Trhr1 ko mice with the leptin-deficient ob/ob mice. Hypothyroid Trhr1/ob double knockout mice showed a blunted response to leptin treatment with respect to body weight and food intake and exhibited a decreased activation of phospho-signal transducer and activator of transcription 3 as well as a up-regulation of suppressor of cytokine signaling 3 upon leptin treatment, particularly in the arcuate nucleus. These data indicate alterations in the intracellular processing of the leptin signal under hypothyroid conditions and thereby unravel a novel mode of action by which TH affects energy metabolism.

scholarly journals Thermoregulatory role of ghrelin in the induction of torpor under a restricted feeding condition

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takahiro Sato ◽  
Kanae Oishi ◽  
Daisuke Koga ◽  
Takanori Ida ◽  
Yusuke Sakai ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Uncoupling Protein ◽  
Restricted Feeding ◽  
Uncoupling Protein 1 ◽  
Feeding Condition ◽  
Nervous System Activity ◽  
Brown Adipose ◽  
Hypothalamic Arcuate Nucleus ◽  
Sympathetic Nervous

AbstractGhrelin, a circulating orexigenic hormone secreted from the stomach, stimulates appetite and food intake by activating the hypothalamic arcuate nucleus. Administration of exogenous ghrelin exerts anabolic effects, causing weight gain, increased adiposity, and decreased metabolism. Body temperature (BT), which is determined by the balance of heat production and heat loss, must be strictly regulated to maintain proper cellular function and metabolism. However, the role of ghrelin in thermoregulation remains unclear. In this study, we found that ghrelin was essential for decreasing BT when mice are placed under calorie restriction. Elevated ghrelin concentrations induced by fasting correlated with significant decreases in BT, a hibernation-like state called torpor. Ghrelin-deficient (Ghrl−/−) animals could not enter torpor. The BT of Ghrl−/− mice also remained high under restricted feeding, but the animals gradually entered precipitous hypothermia, indicating thermoregulatory impairment. These effects of ghrelin on thermoregulation were the result of suppression of sympathetic nervous system activity input to brown adipose tissue; in the absence of ghrelin, it was not possible to suppress uncoupling protein 1 (ucp1) expression and decrease BT in low-energy states. Together, these findings demonstrate that ghrelin is an essential circulating hormone involved in lowering BT.

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