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Статті в журналах з теми "Pro-opiomelanocortin neurons"

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Автор: Grafiati

Опубліковано: 11 травня 2022

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1

Ishikawa, Koicni, Kenji Katakai, Shigeyasu Tanaka, Seiichi Haga, Hiroshi Mochida, and Kouichi Itoh. "Pro-Opiomelanocortin-Containing Neurons in Rat Median Eminence." Neuroendocrinology 56, no. 2 (1992): 178–84. http://dx.doi.org/10.1159/000126226.

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2

Harberson, Mitchell T., and Jennifer W. Hill. "Pro-Opiomelanocortin Neural Activation and Sexual Interest in Male Mice." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A54—A55. http://dx.doi.org/10.1210/jendso/bvab048.109.

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Abstract Pro-opiomelanocortin (POMC) neurons in the hypothalamus play a role in both the control of metabolic state and sexual behavior. Along with the fast neurotransmitters glutamate and/or GABA, POMC neurons secrete cocaine- and amphetamine-regulated transcript (CART) and products of the POMC gene, including β-endorphin and α-melanocortin stimulating hormone (α-MSH). Published data from our lab demonstrate a lack of sexual interest in male mice when both the leptin receptor and insulin receptor are deleted from POMC neurons. Furthermore, this absence of interest correlates with a decrease in the POMC product α-MSH. However, it is not known whether these effects correspond to an increase in POMC neural activation. We hypothesized that activation of POMC neurons in male mice would lead to improved sexual interest. We have crossed mice with cre-dependent expression of the excitatory designer receptor, hM3Dq, with mice expressing cre under control of the POMC promoter. When these mice are administered intraperitoneal clozapine-N-oxide (CNO), POMC neurons exhibit increased activation. We completed a comprehensive mating analysis to measure the sexual desire and erectile and ejaculatory capabilities of these male mice under CNO or saline administration. Additionally, we sacrificed the mice after injection of CNO or saline to perform immunostaining for the protein c-fos as an indicator of neural activation. As expected, activation of POMC neurons with CNO increased c-fos expression, while the impact on male sexual interest was more nuanced. These experiments emphasize the need to investigate the specific neuropeptide and transmitter output by POMC neurons that influences sexual behavior and function.

3

Xu, Yong, Juli E. Jones, Daisuke Kohno, Kevin W. Williams, Charlotte E. Lee, Michelle J. Choi, Jason G. Anderson, et al. "5-HT2CRs Expressed by Pro-Opiomelanocortin Neurons Regulate Energy Homeostasis." Neuron 60, no. 4 (November 2008): 582–89. http://dx.doi.org/10.1016/j.neuron.2008.09.033.

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4

Maolood, N., and B. Meister. "Dynorphin in pro-opiomelanocortin neurons of the hypothalamic arcuate nucleus." Neuroscience 154, no. 3 (June 2008): 1121–31. http://dx.doi.org/10.1016/j.neuroscience.2008.04.011.

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5

Good, Deborah J., Haiyan Zhang, Robert W. Grange, and Thomas Braun. "Pro-opiomelanocortin Neurons and the Transcriptional Regulation of Motivated Exercise." Exercise and Sport Sciences Reviews 48, no. 2 (April 2020): 74–82. http://dx.doi.org/10.1249/jes.0000000000000219.

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6

Pilcher, Webster H., Shirley A. Joseph, and Joseph V. McDonald. "Immunocytochemical localization of pro-opiomelanocortin neurons in human brain areas subserving stimulation analgesia." Journal of Neurosurgery 68, no. 4 (April 1988): 621–29. http://dx.doi.org/10.3171/jns.1988.68.4.0621.

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✓ The distribution of pro-opiomelanocortin (β-endorphin, adrenocorticotropic hormone, and 16-K) neurons and fiber projections was evaluated immunocytochemically in 50-µ thick cryostat sections of human diencephalon and midbrain. Specific attention was focused upon regions in which deep brain stimulation has been most effective in the relief of selected chronic pain syndromes. This study revealed a remarkable, nearly point-to-point correlation between clinically effective stimulation sites and the distribution of pro-opiomelanocortin fibers in the human brain. Of particular interest was the dense innervation of the periventricular stratum along the third ventricle, the parafascicular centromedian region of the thalamus, and the periaqueductal gray matter of the midbrain. This study provides anatomical support for the hypothesis that β-endorphin-containing neuronal systems may contribute to stimulation analgesia in the human.

7

Claret, Marc, Mark A. Smith, Claude Knauf, Hind Al-Qassab, Angela Woods, Amanda Heslegrave, Kaisa Piipari, et al. "Deletion ofLkb1in Pro-Opiomelanocortin Neurons Impairs Peripheral Glucose Homeostasis in Mice." Diabetes 60, no. 3 (January 24, 2011): 735–45. http://dx.doi.org/10.2337/db10-1055.

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8

Mountjoy, Kathleen G. "Functions for pro-opiomelanocortin-derived peptides in obesity and diabetes." Biochemical Journal 428, no. 3 (May 27, 2010): 305–24. http://dx.doi.org/10.1042/bj20091957.

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Melanocortin peptides, derived from POMC (pro-opiomelanocortin) are produced in the ARH (arcuate nucleus of the hypothalamus) neurons and the neurons in the commissural NTS (nucleus of the solitary tract) of the brainstem, in anterior and intermediate lobes of the pituitary, skin and a wide range of peripheral tissues, including reproductive organs. A hypothetical model for functional roles of melanocortin receptors in maintaining energy balance was proposed in 1997. Since this time, there has been an extraordinary amount of knowledge gained about POMC-derived peptides in relation to energy homoeostasis. Development of a Pomc-null mouse provided definitive proof that POMC-derived peptides are critical for the regulation of energy homoeostasis. The melanocortin system consists of endogenous agonists and antagonists, five melanocortin receptor subtypes and receptor accessory proteins. The melanocortin system, as is now known, is far more complex than most of us could have imagined in 1997, and, similarly, the importance of this system for regulating energy homoeostasis in the general human population is much greater than we would have predicted. Of the known factors that can cause human obesity, or protect against it, the melanocortin system is by far the most significant. The present review is a discussion of the current understanding of the roles and mechanism of action of POMC, melanocortin receptors and AgRP (agouti-related peptide) in obesity and Type 2 diabetes and how the central and/or peripheral melanocortin systems mediate nutrient, leptin, insulin, gut hormone and cytokine regulation of energy homoeostasis.

9

Jo, Young-Hwan, Ya Su, Roger Gutierrez-Juarez, and Streamson Chua. "Oleic Acid Directly Regulates POMC Neuron Excitability in the Hypothalamus." Journal of Neurophysiology 101, no. 5 (May 2009): 2305–16. http://dx.doi.org/10.1152/jn.91294.2008.

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The mammalian CNS relies on a constant supply of external glucose for its undisturbed operation. However, neurons can readily switch to using fatty acids and ketones as alternative fuels. Here, we show that oleic acid (OA) excites pro-opiomelanocortin (POMC) neurons by inhibition of ATP-activated potassium (KATP) channels. The involvement of KATP channels is further supported by experiments in SUR1 KO animals. Inhibition of β-oxidation using carnitine palmitoyltransferase-1 inhibitors blocks OA-induced depolarization. The depolarizing effect of OA is specific because it is not mimicked by octanoic acid. Furthermore, OA does not regulate the excitability of agouti-related peptide neurons. High-fat feeding alters POMC neuron excitability, but not its response to OA. Thus β-oxidation in POMC neurons may mediate the appetite-suppressing (anorexigenic) effects of OA.

10

Tang, Qin, Yong Gao, Qinhui Liu, Xuping Yang, Tong Wu, Cuiyuan Huang, Ya Huang, et al. "Sirt6 in pro-opiomelanocortin neurons controls energy metabolism by modulating leptin signaling." Molecular Metabolism 37 (July 2020): 100994. http://dx.doi.org/10.1016/j.molmet.2020.100994.

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11

Cerritelli, Serena, Stefan Hirschberg, Rob Hill, Nina Balthasar, and Anthony E. Pickering. "Activation of Brainstem Pro-opiomelanocortin Neurons Produces Opioidergic Analgesia, Bradycardia and Bradypnoea." PLOS ONE 11, no. 4 (April 14, 2016): e0153187. http://dx.doi.org/10.1371/journal.pone.0153187.

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12

Berglund, Eric D., Chen Liu, Jong-Woo Sohn, Tiemin Liu, Mi Hwa Kim, Charlotte E. Lee, Claudia R. Vianna, Kevin W. Williams, Yong Xu, and Joel K. Elmquist. "Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis." Journal of Clinical Investigation 123, no. 12 (November 1, 2013): 5061–70. http://dx.doi.org/10.1172/jci70338.

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13

Berglund, Eric D., Chen Liu, Jong-Woo Sohn, Tiemin Liu, Mi Hwa Kim, Charlotte E. Lee, Claudia R. Vianna, Kevin W. Williams, Yong Xu, and Joel K. Elmquist. "Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis." Journal of Clinical Investigation 124, no. 4 (April 1, 2014): 1868. http://dx.doi.org/10.1172/jci75669.

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14

Xu, Yong, Eric D. Berglund, Jong-Woo Sohn, William L. Holland, Jen-Chieh Chuang, Makoto Fukuda, Jari Rossi, et al. "5-HT2CRs expressed by pro-opiomelanocortin neurons regulate insulin sensitivity in liver." Nature Neuroscience 13, no. 12 (October 31, 2010): 1457–59. http://dx.doi.org/10.1038/nn.2664.

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15

Yan, Chunling, Yanlin He, Yuanzhong Xu, Gang Shu, Chunmei Wang, Yongjie Yang, Kenji Saito, et al. "Apolipoprotein A-IV Inhibits AgRP/NPY Neurons and Activates Pro-Opiomelanocortin Neurons in the Arcuate Nucleus." Neuroendocrinology 103, no. 5 (August 25, 2015): 476–88. http://dx.doi.org/10.1159/000439436.

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16

Lam, Brian Y. H., Irene Cimino, Joseph Polex-Wolf, Sara Nicole Kohnke, Debra Rimmington, Valentine Iyemere, Nicholas Heeley, et al. "Heterogeneity of hypothalamic pro-opiomelanocortin-expressing neurons revealed by single-cell RNA sequencing." Molecular Metabolism 6, no. 5 (May 2017): 383–92. http://dx.doi.org/10.1016/j.molmet.2017.02.007.

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17

Steyn, Frederik J., Shyuan T. Ngo, Vicky Ping Chen, Lora C. Bailey-Downs, Teresa Y. Xie, Martin Ghadami, Stephen Brimijoin та ін. "17α-estradiol acts through hypothalamic pro-opiomelanocortin expressing neurons to reduce feeding behavior". Aging Cell 17, № 1 (23 листопада 2017): e12703. http://dx.doi.org/10.1111/acel.12703.

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18

Sohn, Jong-Woo, and Kevin W. Williams. "Functional Heterogeneity of Arcuate Nucleus Pro-Opiomelanocortin Neurons: Implications for Diverging Melanocortin Pathways." Molecular Neurobiology 45, no. 2 (February 12, 2012): 225–33. http://dx.doi.org/10.1007/s12035-012-8240-6.

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19

Cawley, Niamh X., Zhaojin Li, and Y. Peng Loh. "60 YEARS OF POMC: Biosynthesis, trafficking, and secretion of pro-opiomelanocortin-derived peptides." Journal of Molecular Endocrinology 56, no. 4 (May 2016): T77—T97. http://dx.doi.org/10.1530/jme-15-0323.

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Анотація:

Pro-opiomelanocortin (POMC) is a prohormone that encodes multiple smaller peptide hormones within its structure. These peptide hormones can be generated by cleavage of POMC at basic residue cleavage sites by prohormone-converting enzymes in the regulated secretory pathway (RSP) of POMC-synthesizing endocrine cells and neurons. The peptides are stored inside the cells in dense-core secretory granules until released in a stimulus-dependent manner. The complexity of the regulation of the biosynthesis, trafficking, and secretion of POMC and its peptides reflects an impressive level of control over many factors involved in the ultimate role of POMC-expressing cells, that is, to produce a range of different biologically active peptide hormones ready for action when signaled by the body. From the discovery of POMC as the precursor to adrenocorticotropic hormone (ACTH) and β-lipotropin in the late 1970s to our current knowledge, the understanding of POMC physiology remains a monumental body of work that has provided insight into many aspects of molecular endocrinology. In this article, we describe the intracellular trafficking of POMC in endocrine cells, its sorting into dense-core secretory granules and transport of these granules to the RSP. Additionally, we review the enzymes involved in the maturation of POMC to its various peptides and the mechanisms involved in the differential processing of POMC in different cell types. Finally, we highlight studies pertaining to the regulation of ACTH secretion in the anterior and intermediate pituitary and POMC neurons of the hypothalamus.

20

Nguyen, Q. T., and E. J. Wagner. "172 ESTROGEN ATTENUATES THE CANNABINOID MODULATION OF GLUTAMATERGIC SYNAPTIC CURRENTS IN PRO-OPIOMELANOCORTIN NEURONS." Journal of Investigative Medicine 54, no. 1 (January 1, 2006): S109.6—S110. http://dx.doi.org/10.2310/6650.2005.x0004.171.

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21

Coupé, Bérengère, Yuko Ishii, Marcelo O. Dietrich, Masaaki Komatsu, Tamas L. Horvath, and Sebastien G. Bouret. "Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation." Cell Metabolism 15, no. 2 (February 2012): 247–55. http://dx.doi.org/10.1016/j.cmet.2011.12.016.

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22

Xiao, Yuzhong, Tingting Xia, Junjie Yu, Yalan Deng, Hao Liu, Bin Liu, Shanghai Chen, Yong Liu та Feifan Guo. "Knockout of inositol-requiring enzyme 1α in pro-opiomelanocortin neurons decreases fat mass via increasing energy expenditure". Open Biology 6, № 8 (серпень 2016): 160131. http://dx.doi.org/10.1098/rsob.160131.

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Although numerous functions of inositol-requiring enzyme 1α (IRE1α) have been identified, a role of IRE1α in pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus is largely unknown. Here, we showed that mice lacking IRE1α specifically in POMC neurons (PIKO) are lean and resistant to high-fat diet-induced obesity and obesity-related insulin resistance, liver steatosis and leptin resistance. Furthermore, PIKO mice had higher energy expenditure, probably due to increased thermogenesis in brown adipose tissue. Additionally, α-melanocyte-stimulating hormone production was increased in the hypothalamus of PIKO mice. These results demonstrate that IRE1α in POMC neurons plays a critical role in the regulation of obesity and obesity-related metabolic disorders. Our results also suggest that IRE1α is not only an endoplasmic reticulum stress sensor, but also a new potential therapeutic target for obesity and obesity-related metabolic diseases.

23

Grossberg, Aaron J., Jarrad M. Scarlett, XinXia Zhu, Darren D. Bowe, Ayesha K. Batra, Theodore P. Braun, and Daniel L. Marks. "Arcuate Nucleus Proopiomelanocortin Neurons Mediate the Acute Anorectic Actions of Leukemia Inhibitory Factor via gp130." Endocrinology 151, no. 2 (February 1, 2010): 606–16. http://dx.doi.org/10.1210/en.2009-1135.

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The proinflammatory cytokine leukemia inhibitory factor (LIF) is induced in disease states and is known to inhibit food intake when administered centrally. However, the neural pathways underlying this effect are not well understood. We demonstrate that LIF acutely inhibits food intake by directly activating pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus. We show that arcuate POMC neurons express the LIF-R, and that LIF stimulates the release of the anorexigenic peptide, α-MSH from ex vivo hypothalami. Transgenic mice lacking gp130, the signal transducing subunit of the LIF-R complex, specifically in POMC neurons fail to respond to LIF. Furthermore, LIF does not stimulate the release of α-MSH from the transgenic hypothalamic explants. These findings indicate that POMC neurons mediate the acute anorectic actions of central LIF administration and provide a mechanistic link between inflammation and food intake.

24

Stump, Madeliene, Deng-Fu Guo, Ko-Ting Lu, Masashi Mukohda, Xuebo Liu, Kamal Rahmouni та Curt D. Sigmund. "Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance". Physiological Genomics 48, № 7 (1 липня 2016): 491–501. http://dx.doi.org/10.1152/physiolgenomics.00032.2016.

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Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

25

Pritchard, LE, AV Turnbull, and A. White. "Pro-opiomelanocortin processing in the hypothalamus: impact on melanocortin signalling and obesity." Journal of Endocrinology 172, no. 3 (March 1, 2002): 411–21. http://dx.doi.org/10.1677/joe.0.1720411.

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Bioactive peptides derived from the prohormone, pro-opiomelanocortin (POMC), are generated in neurons of the hypothalamus and act as endogenous ligands for the melanocortin-4 receptor (MC4R), a key molecule underlying appetite control and energy homeostasis. It is therefore important to understand many aspects of POMC gene regulation in the brain, as pharmacological manipulation of POMC expression/processing could be a potential strategy to combat obesity. Most studies that have analysed POMC gene expression in the hypothalamus have focused on gene transcription experiments. Ultimately, however, factors that regulate post-translational processing and secretion of peptides will have most bearing on melanocortin signalling. This article focuses on (a) current evidence that POMC is involved in obesity, (b) how POMC transcription is regulated in the hypothalamus, (c) the mechanism by which proteolytic processing of POMC is controlled in the hypothalamus and what peptides are produced and (d) which POMC-derived peptides are the most potent ligands at the melanocortin receptor in vitro and in vivo. It seems that post-translational cleavage of POMC in the hypothalamus may be regulated with respect to energy requirement. We predict that further research into hypothalamic POMC processing, and the proteolytic enzymes involved, may yield important new clues on how flux through the MC4R pathway is regulated.

26

Wang, Liheng, Lina Sui, Sunil K. Panigrahi, Kana Meece, Yurong Xin, Jinrang Kim, Jesper Gromada, et al. "PC1/3 Deficiency Impacts Pro-opiomelanocortin Processing in Human Embryonic Stem Cell-Derived Hypothalamic Neurons." Stem Cell Reports 8, no. 2 (February 2017): 264–77. http://dx.doi.org/10.1016/j.stemcr.2016.12.021.

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27

Sohn, Jong-Woo, Yong Xu, Juli E. Jones, Kevin Wickman, Kevin W. Williams, and Joel K. Elmquist. "Serotonin 2C Receptor Activates a Distinct Population of Arcuate Pro-opiomelanocortin Neurons via TRPC Channels." Neuron 71, no. 3 (August 2011): 488–97. http://dx.doi.org/10.1016/j.neuron.2011.06.012.

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28

Jamali, Khalid A., and Gérard Tramu. "Adrenalectomy does not affect the nocturnal peak of fos expression within hypothalamic pro-opiomelanocortin neurons." Biology of the Cell 89, no. 9 (December 1997): 579–85. http://dx.doi.org/10.1111/j.1768-322x.1997.tb01035.x.

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29

Chowen, Julie A., Jesús Argente, Linda Vician, Donald K. Clifton, and Robert A. Steiner. "Pro-Opiomelanocortin Messenger RNA in Hypothalamic Neurons Is Increased by Testosterone through Aromatization to Estradiol." Neuroendocrinology 52, no. 6 (1990): 581–88. http://dx.doi.org/10.1159/000125647.

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30

Leyrer-Jackson, Jonna M., Lauren E. Hood, and M. Foster Olive. "Alcohol consumption preferentially activates a subset of pro-opiomelanocortin (POMC) producing neurons targeting the amygdala." Neuropharmacology 195 (September 2021): 108674. http://dx.doi.org/10.1016/j.neuropharm.2021.108674.

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31

Resch, Jon M., Joanne P. Boisvert, Allison E. Hourigan, Christopher R. Mueller, Sun Shin Yi, and SuJean Choi. "Stimulation of the hypothalamic ventromedial nuclei by pituitary adenylate cyclase-activating polypeptide induces hypophagia and thermogenesis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 6 (December 2011): R1625—R1634. http://dx.doi.org/10.1152/ajpregu.00334.2011.

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Numerous studies have demonstrated that the hypothalamic ventromedial nuclei (VMN) regulate energy homeostasis by integrating and utilizing behavioral and metabolic mechanisms. The VMN heavily express pituitary adenylate cyclase-activating polypeptide (PACAP) type I receptors (PAC1R). Despite the receptor distribution, most PACAP experiments investigating affects on feeding have focused on intracerebroventricular administration or global knockout mice. To identify the specific contribution of PACAP signaling in the VMN, we injected PACAP directly into the VMN and measured feeding behavior and indices of energy expenditure. Following an acute injection of PACAP, nocturnal food intake was significantly reduced for 6 h after injections without evidence of malaise. In addition, PACAP-induced suppression of feeding also occurred following an overnight fast and could be blocked by a specific PAC1R antagonist. Metabolically, VMN-specific injections of PACAP significantly increased both core body temperature and spontaneous locomotor activity with a concurrent increase in brown adipose uncoupling protein 1 mRNA expression. To determine which signaling pathways were responsive to PACAP administration into the VMN, we measured mRNA expression of well-characterized hypothalamic neuropeptide regulators of feeding. One hour after PACAP administration, expression of pro-opiomelanocortin mRNA was significantly increased in the arcuate nuclei (ARC), with no changes in neuropeptide Y and agouti-related polypeptide mRNA levels. This suggests that PAC1R expressing VMN neurons projecting to pro-opiomelanocortin neurons contribute to hypophagia by involving melanocortin signaling. While the VMN also abundantly express PACAP protein, the present study demonstrates that PACAP input to the VMN can influence the control of energy homeostasis.

32

Chen, Weijie, Zhibo Yan, Shaozhuang Liu, Guangyong Zhang, Dong Sun, and Sanyuan Hu. "The Changes of Pro-opiomelanocortin Neurons in Type 2 Diabetes Mellitus Rats After Ileal Transposition: The Role of POMC Neurons." Journal of Gastrointestinal Surgery 15, no. 9 (June 30, 2011): 1618–24. http://dx.doi.org/10.1007/s11605-011-1606-7.

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33

Shu, I.-Wei, Daniel L. Lindenberg, Tooru M. Mizuno, James L. Roberts, and Charles V. Mobbs. "The fatty acid synthase inhibitor cerulenin and feeding, like leptin, activate hypothalamic pro-opiomelanocortin (POMC) neurons." Brain Research 985, no. 1 (September 2003): 1–12. http://dx.doi.org/10.1016/s0006-8993(03)02806-3.

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34

Jang, Pil-Geum, Cherl Namkoong, Gil Myoung Kang, Man-Wook Hur, Seung-Whan Kim, Geun Hyang Kim, Yeoungsup Kang та ін. "NF-κB Activation in Hypothalamic Pro-opiomelanocortin Neurons Is Essential in Illness- and Leptin-induced Anorexia". Journal of Biological Chemistry 285, № 13 (22 січня 2010): 9706–15. http://dx.doi.org/10.1074/jbc.m109.070706.

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35

Knigge, Ulrich, Steen Matzen, Flemming W. Bach, Peter Bang, and Jørgen Warberg. "Involvement of histaminergic neurons in the stress-induced release of pro-opiomelanocortin-derived peptides in rats." Acta Endocrinologica 120, no. 4 (April 1989): 533–39. http://dx.doi.org/10.1530/acta.0.1200533.

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Abstract. Histamine, which acts as a neurotransmitter, stimulates the release of the pro-opiomelanocortin derived peptides ACTH, β-lipotropin, and β-endorphin. Since stress affects the hypothalamic turn-over of neuronal histamine, we investigated the role of histaminergic neurons in the mediation of the stress-induced release of ACTH and β-endorphin immunoreactivity in male rats. In control animals histamine receptor antagonists had no effect on the release of ACTH or β-endorphin immunoreactivity. Restraint and ether stress increased plasma ACTH 3- and 2-fold, respectively. The responses were almost prevented by intracerebroventricular or intra-arterial infusion of the H2-receptor antagonists cimetidine and ranitidine. Infused intracerebroventricularly the H1-receptor antagonist mepyramine inhibited the ACTH response to restraint by 45% (P< 0.01), but had no effect on the response to ether. Infused intra-arterially the H1-receptor antagonists mepyramine or SKF-93944 had no effect. Restraint and ether stress increased plasma β-endorphin immunoreactivity 6- and 5-fold, respectively. Sephadex G-50 gel chromatography of plasma showed that the β-endorphin immunoreactivity in stressed rats coeluted with β-lipotropin and β-endorphin, whereas the immunoreactivity in control animals co-eluted almost exclusively with β-endorphin. The H2-receptor antagonists cimetidine and ranitidine infused intracerebroventricurlarly inhibited the responses of β-endorphin immunoreactivity to restraint and ether stress by 90 and 70%, respectively, whereas intra-arterial infusion of these antagonists inhibited the responses by only 50 and 60%, respectively. The H1-receptor antagonist mepyramine infused intracerebroventricularly inhibited the β-endorphin immunoreactivity response to restraint and ether stress by 40 and 25%, respectively, whereas intra-arterial infusion of mepyramine or the other H1-receptor antagonist SKF-93944 prevented the response to restraint stress, but had no effect on the response to ether stress. We suggest that hypothalamic histamine is involved in the mediation of the stress-induced release of the proopiomelanocortin-derived peptides ACTH, β-endorphin and β-lipotropin. The effect is mediated preferentially via H2-receptors, but H1-receptors may also play a role.

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Rorato, Rodrigo, Aline Motta Menezes, Alexandre Giusti-Paiva, Margaret De Castro, José Antunes-Rodrigues, and Lucila Leico Kagohara Elias. "Prostaglandin mediates endotoxaemia-induced hypophagia by activation of pro-opiomelanocortin and corticotrophin-releasing factor neurons in rats." Experimental Physiology 94, no. 3 (February 13, 2009): 371–79. http://dx.doi.org/10.1113/expphysiol.2008.045435.

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37

Chen, Shao-Rui, Hong Chen, Jing-Jing Zhou, Geetali Pradhan, Yuxiang Sun, Hui-Lin Pan, and De-Pei Li. "Ghrelin receptors mediate ghrelin-induced excitation of agouti-related protein/neuropeptide Y but not pro-opiomelanocortin neurons." Journal of Neurochemistry 142, no. 4 (June 21, 2017): 512–20. http://dx.doi.org/10.1111/jnc.14080.

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38

Fremeau, Robert T., Dominic J. Autelitano, Mariann Blum, Josiah Wilcox, and James L. Roberts. "Intervening sequence-specific in situ hybridization: detection of the pro-opiomelanocortin gene primary transcript in individual neurons." Molecular Brain Research 6, no. 2-3 (November 1989): 197–201. http://dx.doi.org/10.1016/0169-328x(89)90054-5.

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Hill, Jennifer W., Carol F. Elias, Makoto Fukuda, Kevin W. Williams, Eric D. Berglund, William L. Holland, You-Ree Cho, et al. "Direct Insulin and Leptin Action on Pro-opiomelanocortin Neurons Is Required for Normal Glucose Homeostasis and Fertility." Cell Metabolism 11, no. 4 (April 2010): 286–97. http://dx.doi.org/10.1016/j.cmet.2010.03.002.

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Qiu, Lianglin, Minjie Chen, Xiaoke Wang, Sufang Chen та Zhekang Ying. "PM2.5 Exposure of Mice during Spermatogenesis: A Role of Inhibitor κB Kinase 2 in Pro-Opiomelanocortin Neurons". Environmental Health Perspectives 129, № 9 (вересень 2021): 097006. http://dx.doi.org/10.1289/ehp8868.

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41

Landry, Taylor, Daniel Shookster, Alec Chaves, Katrina Free, Tony Nguyen, and Hu Huang. "Exercise increases NPY/AgRP and TH neuron activity in the hypothalamus of female mice." Journal of Endocrinology 252, no. 3 (March 1, 2022): 167–77. http://dx.doi.org/10.1530/joe-21-0250.

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Recent evidence identifies a potent role for aerobic exercise to modulate the activity of hypothalamic neurons related to appetite; however, these studies have been primarily performed in male rodents. Since females have markedly different neuronal mechanisms regulating food intake, the current study aimed to determine the effects of acute treadmill exercise on hypothalamic neuron populations involved in regulating appetite in female mice. Mature, untrained female mice were exposed to acute sedentary, low- (10 m/min), moderate- (14 m/min), and high (18 m/min)-intensity treadmill exercise in a randomized crossover design. Mice were fasted 10 h before exercise, and food intake was monitored for 48 h after bouts. Immunohistochemical detection of cFOS was performed 3 h post-exercise to determine the changes in hypothalamic neuropeptide Y (NPY)/agouti-related peptide (AgRP), pro-opiomelanocortin (POMC), tyrosine hydroxylase (TH), and SIM1-expressing neuron activity concurrent with the changes in food intake. Additionally, stains for pSTAT3tyr705 and pERKthr202/tyr204 were performed to detect exercise-mediated changes in intracellular signaling. Briefly, moderate- and high-intensity exercises increased 24-h food intake by 5.9 and 19%, respectively, while low-intensity exercise had no effects. Furthermore, increases in NPY/AgRPARC, SIM1PVN, and TH neuron activity were observed 3 h after high-intensity exercise, with no effects on POMCARC neurons. While no effects of exercise on pERKthr202/tyr204 were observed, pSTAT3tyr705 was elevated specifically in NPY/AgRP neurons 3 h post-exercise. Overall, aerobic exercise increased the activity of several appetite-stimulating neuron populations in the hypothalamus of female mice, which may provide insight into previously reported sexual dimorphisms in post-exercise feeding.

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Laing, Brenton T., Khoa Do, Tomoko Matsubara, David W. Wert, Michael J. Avery, Erin M. Langdon, Donghai Zheng, and Hu Huang. "Voluntary exercise improves hypothalamic and metabolic function in obese mice." Journal of Endocrinology 229, no. 2 (May 2016): 109–22. http://dx.doi.org/10.1530/joe-15-0510.

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Exercise plays a critical role in regulating glucose homeostasis and body weight. However, the mechanism of exercise on metabolic functions associated with the CNS has not been fully understood. C57BL6 male mice (n=45) were divided into three groups: normal chow diet, high-fat diet (HFD) treatment, and HFD along with voluntary running wheel exercise training for 12 weeks. Metabolic function was examined by the Comprehensive Lab Animal Monitoring System and magnetic resonance imaging; phenotypic analysis included measurements of body weight, food intake, glucose and insulin tolerance tests, as well as insulin and leptin sensitivity studies. By immunohistochemistry, the amount changes in the phosphorylation of signal transducer and activator of transcription 3, neuronal proliferative maker Ki67, apoptosis positive cells as well as pro-opiomelanocortin (POMC)-expressing neurons in the arcuate area of the hypothalamus was identified. We found that 12 weeks of voluntary exercise training partially reduced body weight gain and adiposity induced by an HFD. Insulin and leptin sensitivity were enhanced in the exercise training group verses the HFD group. Furthermore, the HFD-impaired POMC-expressing neuron is remarkably restored in the exercise training group. The restoration of POMC neuron number may be due to neuroprotective effects of exercise on POMC neurons, as evidenced by altered proliferation and apoptosis. In conclusion, our data suggest that voluntary exercise training improves metabolic symptoms induced by HFD, in part through protected POMC-expressing neuron from HFD and enhanced leptin signaling in the hypothalamus that regulates whole-body energy homeostasis.

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Jamali, Khalid A., Marc Corio, Pierrette Dubourg, Charlène Thenailler, and Gérard Tramu. "The daily pattern of Fos synthesis by hypothalamic pro-opiomelanocortin neurons is unaffected by adrenalectomy in the rat." Neuroscience Letters 250, no. 2 (June 1998): 119–22. http://dx.doi.org/10.1016/s0304-3940(98)00446-7.

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44

Plum, Leona, Hua V. Lin, Roxanne Dutia, Jun Tanaka, Kumiko S. Aizawa, Michihiro Matsumoto, Andrea J. Kim, et al. "The obesity susceptibility gene Cpe links FoxO1 signaling in hypothalamic pro-opiomelanocortin neurons with regulation of food intake." Nature Medicine 15, no. 10 (September 20, 2009): 1195–201. http://dx.doi.org/10.1038/nm.2026.

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45

Bruder-Nascimento, Thiago, Simone Kennard, Galina Antonova, James D. Mintz, Kendra K. Bence та Eric J. Belin de Chantemèle. "Ptp1b deletion in pro-opiomelanocortin neurons increases energy expenditure and impairs endothelial function via TNF-α dependent mechanisms". Clinical Science 130, № 11 (22 квітня 2016): 881–93. http://dx.doi.org/10.1042/cs20160073.

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The present study suggests that although increasing energy expenditure might be an efficient therapy to reduce body weight and prevent diabetes, it might have deleterious effects on the cardiovascular system and notably promotes the development of vascular dysfunction.

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Kiss, József, Zsolt Csaba, Ágnes Csáki, and Béla Halász. "Glutamatergic innervation of neuropeptide Y and pro-opiomelanocortin-containing neurons in the hypothalamic arcuate nucleus of the rat." European Journal of Neuroscience 21, no. 8 (April 2005): 2111–19. http://dx.doi.org/10.1111/j.1460-9568.2005.04012.x.

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47

Smith, Mark A., Loukia Katsouri, Samuel Virtue, Agharul I. Choudhury, Antonio Vidal-Puig, Michael L. J. Ashford, and Dominic J. Withers. "Calcium Channel CaV2.3 Subunits Regulate Hepatic Glucose Production by Modulating Leptin-Induced Excitation of Arcuate Pro-opiomelanocortin Neurons." Cell Reports 25, no. 2 (October 2018): 278–87. http://dx.doi.org/10.1016/j.celrep.2018.09.024.

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48

De Bond, Julie-Ann P., and Jeremy T. Smith. "Kisspeptin and energy balance in reproduction." REPRODUCTION 147, no. 3 (March 2014): R53—R63. http://dx.doi.org/10.1530/rep-13-0509.

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Kisspeptin is vital for the neuroendocrine regulation of GNRH secretion. Kisspeptin neurons are now recognized as a central pathway responsible for conveying key homeostatic information to GNRH neurons. This pathway is likely to mediate the well-established link between energy balance and reproductive function. Thus, in states of severely altered energy balance (either negative or positive), fertility is compromised, as isKiss1expression in the arcuate nucleus. A number of metabolic modulators have been proposed as regulators of kisspeptin neurons including leptin, ghrelin, pro-opiomelanocortin (POMC), and neuropeptide Y (NPY). Whether these regulate kisspeptin neurons directly or indirectly will be discussed. Moreover, whether the stimulatory role of leptin on reproduction is mediated by kisspeptin directly will be questioned. Furthermore, in addition to being expressed in GNRH neurons, the kisspeptin receptor (Kiss1r) is also expressed in other areas of the brain, as well as in the periphery, suggesting alternative roles for kisspeptin signaling outside of reproduction. Interestingly, kisspeptin neurons are anatomically linked to, and can directly excite, anorexigenic POMC neurons and indirectly inhibit orexigenic NPY neurons. Thus, kisspeptin may have a direct role in regulating energy balance. Although data fromKiss1rknockout and WT mice found no differences in body weight, recent data indicate that kisspeptin may still play a role in food intake and glucose homeostasis. Thus, in addition to regulating reproduction, and mediating the effect of energy balance on reproductive function, kisspeptin signaling may also be a direct regulator of metabolism.

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Guillod-Maximin, E., A. F. Roy, C. M. Vacher, A. Aubourg, V. Bailleux, A. Lorsignol, L. Pénicaud, M. Parquet, and M. Taouis. "Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons." Journal of Endocrinology 200, no. 1 (October 24, 2008): 93–105. http://dx.doi.org/10.1677/joe-08-0348.

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Adiponectin is involved in the control of energy homeostasis in peripheral tissues through Adipor1 and Adipor2 receptors. An increasing amount of evidence suggests that this adipocyte-secreted hormone may also act at the hypothalamic level to control energy homeostasis. In the present study, we observed the gene and protein expressions of Adipor1 and Adipor2 in rat hypothalamus using different approaches. By immunohistochemistry, Adipor1 expression was ubiquitous in the rat brain. By contrast, Adipor2 expression was more limited to specific brain areas such as hypothalamus, cortex, and hippocampus. In arcuate and paraventricular hypothalamic nuclei, Adipor1, and Adipor2 were expressed by neurons and astrocytes. Furthermore, using transgenic green fluorescent protein mice, we showed that Adipor1 and Adipor2 were present in pro–opiomelanocortin (POMC) and neuropeptide Y (NPY) neurons in the arcuate nucleus. Finally, adiponectin treatment by intracerebroventricular injection induced AMP-activated protein kinase (AMPK) phosphorylation in the rat hypothalamus. This was confirmed byin vitrostudies using hypothalamic membrane fractions. In conclusion, Adipor1 and Adipor2 are both expressed by neurons (including POMC and NPY neurons) and astrocytes in the rat hypothalamic nuclei. Adiponectin is able to increase AMPK phosphorylation in the rat hypothalamus. These data reinforced a potential role of adiponectin and its hypothalamic receptors in the control of energy homeostasis.

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Léger, Lucienne, Zehui Zheng, Chantal Bonnet, and Raymond Cespuglio. "Ultrastructural relationships of the pro-opiomelanocortin axons with the serotoninergic neurons in the dorsal raphe nucleus of the rat." Neuroscience Letters 222, no. 3 (February 1997): 155–58. http://dx.doi.org/10.1016/s0304-3940(97)13363-8.

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