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World Journal of Gastroenterology 2008年第41期14卷 6347-6354页

作者： Daisuke Kohno Shigetomo Suyama Toshihiko Yada Division of Integrative Physiology Department of Physiology Jichi Medical University School of Medicine Yakushiji 3311-1 Shimotsuke

AIM： To explore the mechanism for interactions of leptin with ghrelin and orexin in the arcuate nucleus （ARC） activating neuropeptide Y （NPY） neurons during physiological regulation of feeding, METHODS： Single neurons from ARC of adult rats with matured feeding function were isolated. [Ca2＋]i was measured to monitore their activities. The time course of leptin effects on ghrelin-induced versus orexin-induced [Ca2＋]i increases in NPY neurons was studied. RESULTS： Administration of ghrelin or orexin-A at 101~ mol/L increased cytosolic Ca2~ concentration （[Ca2＋]~） in NPY neurons isolated from the ARC of adult rats. Upon administration of leptin at 10^-14-10^-12 mol/L, ghrelin-induced [Ca2＋]i increases were initially （〈 10 min） inhibited but later restored, exhibiting a transient pattern of inhibition. In contrast, orexin-induced [Ca2＋]i increases were inhibited by leptin in a long- lasting manner. Furthermore, a prior administration of leptin inhibited orexin action but not ghrelin action to increase ICa 2＋li, CONCLUSION： Leptin counteracted ghrelin effects transiently and orexin effects long-lastingly in NPY neurons. The transient property with which leptin counteracts ghrelin action in NPY neurons may allow the fasting-associated increase in ghrelin levels to activate NPY neurons in the presence of physiological leptin and to stimulate feeding.

关键词： Leptin Ghrelin Orexin arcuate nucleus Neuropeptide Y Ca2+ Feeding Phosphatidylinositol 3-kinase Phosphodiesterase 3 Signal transducer and activator of transcription 3

Changes in beta-endorphin neuron numbers and serum hormone levels in the arcuate nucleus of ovariectomized rats undergoing treadmill exercise

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Neural Regeneration Research 2008年第11期3卷 1208-1211页

作者： Weijie Zhang Xiyi Liu Sports Institute of Linyi Normal University Linyi 276005 Shandong Province China Department of Physiology Guangdong Medical College Zhanjiang 524023 Guangdong Province China

BACKGROUND： The arcuate nucleus, when damaged in young rats, can lead to pathological changes in adults, such as osteoporosis. Ovariectomized rats suffer from osteoporosis at eight weeks following surgery and the number of β -endorphin immunoreactive neurons in the arcuate nucleus of the hypothalamus is significantly decreased. OBJECTIVE： To establish a rat model of osteoporosis using ovariectomy and to explore changes in the number of β-endorphin neurons and to correlate any such change with serum hormone levels in response to exercise or rest. DESIGN, TIME AND SETTING： The completely randomized block design, neural morphology study was performed at the Key Laboratory of Physiology, Guangdong Medical College, China between March 2004 and January 2005. MATERIALS： Sixteen healthy female rats were selected for ovariectomy. METHODS： Following model establishment, rats were assigned to either rest or exercise groups and each rat was housed individually. Rats in the exercise group underwent an exercise regimen using a treadmill. MAIN OUTCOME MEASURES： Eight weeks following exercise, radioimmunoassay was performed to detect serum growth hormone, estrogen and osteocalcin levels. Immunohistochemistry was used to measure changes in the number of β -endorphin neurons in the arcuate nucleus of the hypothalamus. Changes in bone metabolism were assessed using bone histomorphometry. RESULTS： In the exercise group, the β -endorphin immunoreactive neurons were high in number, darkly stained, and the nucleus was not obvious. In the rest group, the β -endorphin immunoreactive neurons were low in number and lightly stained. The number of β-endorphin immunoreactive neurons in the exercise group was higher compared with the rest group （t = 2.83, P 〈 0.05）. Estrogen levels were similar between the rest and exercise groups （P 〉 0.05）. Serum osteocalcin and growth hormone levels were significantly higher in the exercise group compared with the rest group （t = 2.78, 2.32, P 〈 0.05）. Compare

关键词： exercise arcuate nucleus β-endorphin immunoreactive neurons ovariectomy osteoporosis

Expression of Kisspeptin/kiss1r System is Down-regulated in the Hypothalamic arcuate nucleus of Pubertal Male Rats with High-fat-diet

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Journal of Reproduction and Contraception 2014年第1期25卷 1-11页

作者： Ran-ran LIU Heng LI Dong-mei ZHANG Yao-feng LV Xiang-yun LIN Hong-qin ZHANG Department of Histology and Embryology Binzhou Medical College Department of Immunology and Microbiology Binzhou Medical College Department of Gynecology and Obstetrics Affiliated Hospital of Binzhou Medical College

Objective To explore the potential function of nutrition on kisspeptin/kisspeptin receptor （kisslr） system in the arcuate nucleus （ARC） of male rats. Methods Pregnant rats were obtained and male pups were used to establish obesity model. Body parameters and blood samples were evaluated. Immunohistochemistry was used to determine the localizations and protein levels of kisspeptin, kisslr, and leptin receptor （LepR） immunoreactivity （IR） in ARC. QRT-PCR was used to determine kissl-, kisslr-, LepR-, and GnRH-mRNA levels. Results The establishment of obesity model was successful as body parameters and hormones levels changed noticeably. Kisspeptin-, kisslr-, and LepR-IR were detected and protein levels decreased significantly in high-fat-diets （HFD） rats than controls. The mRNA levels of kissl, LepR and GnRH significantly decreased in the ARC of HFD-fed rats. No difference was observed in kisslr mRNA levels between the two groups. Conclusion These data suggest that failure to increase GnRH levels with HFD may be associated with pubertal down-regulation of LepR and kisspeptin/kisslr system in the ARC of male rats.

关键词： obesity kisspeptin/kisspeptin receptor (kisslr) system arcuate nucleus puberty leptin receptor

Upregulation of cystathionine β-synthetase in arcuate nucleus produces pain hypersensitivity via PKC-mediated phosphorylation of GluN2B in rats with chronic pancreatitis

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Upregulation of cystathionine β-synthetase in arcuate nucle...

促生长素抑制素样免疫反应在大白鼠弓状核和正中隆起的超微结构分布

中国生理学会消化与营养专业委员会成立大会暨第一届学术会议

作者： Hang Zheng Hongyan Zhu Xiaoyu Zhang Meng Wang Ying Xiao 徐广银 Xinghong Jiang Key Laboratory of Pain Basic Research and Clinical Therapy Department of Neurohiology & Physiology Medical College Institute of Neuroscience Soochow University 苏州大学神经科学研究所

Hydrogen sulfide(HS)contributes to visceral hyperalgesia in primary sensory neurons but its role in central nerve system remains largely *** study was to investigate the roles and underlying mechanisms of HS and its endogenous synthesizing enzymes in arcuate nucleus(ARC)in the pancreatic hyperalgesia in rats with chronic pancreatitis(CP).CP was induced in male adult rats by intraductal injection of trinitrobenzene sulfonic acid(TNBS).Abdominal hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat *** blot analysis was performed to detect protein *** microinjection of O-(Carboxymcthyl)hydroxylaminc hemihydrochloride(AOAA)an inhibitor of cystathionineβ-synthetase(CBS)significantly attenuated abdominal pain in CP rats in a dose-dependent *** of CBS in ARC was markedly uprcgulated while the expression of cystathionine-γ-lyase was not allcred4 weeks after TNBS *** the expression of total GluN2B was not altered TNBS injection greatly enhanced the phosphorylation level of GluN2B in ARC in CP rats when compared with age and sex-matched control *** also significantly increased expression of protein kinase Cy(PKCγ)in *** of AOAAinto ARC reversed the upregulation of p-GluN2B and PKCγin ARC in CP *** the specific PKC inhibitor chelerythrine significantly suppressed p-GluN2B expressionand attenuated abdominal hyperalgesia of CP *** together our data suggest that upregulation of CBS leads to an activation of GluN2B which is likely mediated by PKCγin ARC thus playing an important role in generation of pain hypersensitivity of chronic pancreatitis.

关键词： arcuate nucleus Chronic pancreatitis Abdominal pain Hydrogen sulfide NMDA receptor Protein kinase C

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动物学报 1985年第4期34卷 344-347,396页

作者：朱长庚邓德忠刘庆莹卢金活朱家祥武汉医学院解剖学教研室

本文用免疫电镜方法证明:促生长素抑制素样免疫反应神经末梢分布于弓状棱并与未标记的树突形成轴树突触。在正中隆起的纤维层和栅状层内均可见上述免疫反应末梢,大多数紧贴门脉毛细血管基底膜周围甚至穿入基底膜内。免疫反应末梢尚可与... 详细信息

本文用免疫电镜方法证明:促生长素抑制素样免疫反应神经末梢分布于弓状棱并与未标记的树突形成轴树突触。在正中隆起的纤维层和栅状层内均可见上述免疫反应末梢,大多数紧贴门脉毛细血管基底膜周围甚至穿入基底膜内。免疫反应末梢尚可与未标记的末梢形成轴轴突触样结构。

关键词： Hypothalamus Somatostatin Immunocytochemistry arcuate nucleus Median eminence.

Loss of the centrosomal protein Cenpj leads to dysfunction of the hypothalamus and obesity in mice

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Science China(Life Sciences) 2021年第3期64卷 419-433页

作者： Wenyu Ding Changjiang Zhang Baisong Wang Xin Zhou Le Sun Suijuan Zhong Jing Liu Junjing Zhang Xiaoqun Wang Qian Wu State Key Laboratory of Cognitive Neuroscience and Learning Beijing Normal UniversityBeijing 100875China IDG/McGovern Institute for Brain Research Beijing Normal UniversityBeijing 100875China State Key Laboratory of Brain and Cognitive Science CAS Center for Excellence in Brain Science and Intelligence TechnologyInstitute of Brain-Intelligence Technology(Shanghai)Institute of BiophysicsChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China Advanced Innovation Center for Human Brain Protection Beijing Institute for Brain DisordersCapital Medical UniversityBeijing 100069China

Cenpj is a centrosomal protein located at the centrosomes and the base of cilia,it plays essential roles in regulating neurogenesis and cerebral cortex *** centrosomal and cilium dysfunction are one of the causes of obesity,insulin resistance,and type 2 diabetes,the role that Cenpj plays in the regulation of body weight remains ***,we deleted Cenpj by crossing Cenpjflox/flox mice with Nkx2.1-Cre *** of the centrosomal protein Cenpj in Nkx2.1-expressing cells causes morbid obesity in mice at approximately 4 months of age with expended brain ventricles but no change of brain *** found that hypothalamic cells exhibited reduced proliferation and increased apoptosis upon Cenpj depletion at the embryonic stages,resulting in a dramatic decrease in the number of Proopiomelanocortin(POMC)neurons and electrophysiological dysfunction of NPY neurons in the arcuate nucleus(ARC)in ***,depletion of Cenpj also reduced the neuronal projection from the ARC to the paraventricular nucleus(PVN),with decreased melanocortin-4 receptors(MC4R)expression in PVN *** study defines the roles that Cenpj plays in regulating hypothalamus development and body weight,providing a foundation for further understanding of the pathological mechanisms of related diseases.

关键词： arcuate nucleus centrosomal protein Cenpj Nkx2.1 hypothalamus paraventricular nucleus

nr0b1(DAX1) loss of function in zebrafish causes hypothalamic defects via abnormal progenitor proliferation and differentiation

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Journal of Genetics and Genomics 2022年第3期49卷 217-229页

作者： Wei Zhang Yan Li Sijie Chen Cuizhen Zhang Lili Chen Gang Peng State Key Laboratory of Medical Neurobiology MOE Frontiers Center for Brain ScienceInstitutes of Brain ScienceFudan UniversityShanghai 200032China Department of Endocrinology Huashan HospitalFudan UniversityShanghai 200040China

The nuclear receptor DAX-1, encoded by the NR0B1 gene, is presented in the hypothalamic tissues in humans and other vertebrates. Human patients with NR0B1 mutations often have hypothalamic-pituitary defects, but the involvement of NR0B1 in hypothalamic development and function is not well understood. Here, we report the disruption of the nr0b1 gene in zebrafish causes abnormal expression of gonadotropins, a reduction in fertilization rate, and an increase in postfasting food intake, which are indicators of abnormal hypothalamic functions. We find that loss of nr0b1 increases the number of prodynorphin(pdyn)-expressing neurons but decreases the number of pro-opiomelanocortin(pomcb)-expressing neurons in the zebrafish hypothalamic arcuate region(ARC). Further examination reveals that the proliferation of progenitor cells is reduced in the hypothalamus of nr0b1 mutant embryos accompanying the decreased expression of genes in the Notch signaling pathway. Additionally, the inhibition of Notch signaling in wildtype embryos increases the number of pdyn neurons, mimicking the nr0b1 mutant phenotype. In contrast,ectopic activation of Notch signaling in nr0b1 mutant embryos decreases the number of pdyn *** together, our results suggest that nr0b1 regulates neural progenitor proliferation and maintenance to ensure normal hypothalamic neuron development.

关键词： nr0b1 DAX-1 Hypogonadism Feeding arcuate nucleus Neural progenitor

Feeding behavior and gene expression of appetite-related neuropeptides in mice lacking for neuropeptide Y Y5 receptor subclass

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World Journal of Gastroenterology 2008年第41期14卷 6312-6317页

作者： Hiroshi Higuchi Takeshi Niki Tomohiro Shiiya Division of Pharmacology Niigata University Graduate School of Medical and Dental Sciences

Neuropeptide Y (NPY) is a potent neurotransmitter for feeding. Besides NPY, orexigenic neuropeptides such as agouti-related protein (AgRP), and anorexi- genic neuropeptides such as α-melatonin stimulating hormone (MSH) and cocaine-amphetamine-regulated transcript (CART) are also involved in central feeding regulation. During fasting, NPY and AgRP gene expressions are up-regulated and POMC and CART gene ex- pressions are down-regulated in hypothalamus. Based on the network of peptidergic neurons, the former are involved in positive feeding regulation, and the latter are involved in negative feeding, which exert these feeding-regulated peptides especially in paraventricular nucleus (PVN). To clarify the compensatory mecha- nism of knock-out of NPY system on feeding, change in gene expressions of appetite-related neuropeptides and the feeding behavior was studied in NPY Y5-KO mice. Food intake was increased in Y5-KO mice. Fasting increased the amounts of food and water intake in the KO mice more profoundly. These data indicated the compensatory phenomenon of feeding behavior in Y5-KO mice. RT-PCR and ISH suggested that the compensation of feeding is due to change in gene expressions of AgRP, CART and POMC in hypothalamus. Thus, these fi ndings indicated that the compensatory mechanism involves change in POMC/CART gene expression in arcuate nucleus (ARC). The POMC/CART gene expression is important for central compensatory regulation in feeding behavior.

关键词： Neuropeptide Y Y5 receptor Feeding arcuate nucleus Knockout mice

Kisspeptin regulates gonadotropin-releasing hormone secretion in gonadotropin-releasing hormone/enhanced green fluorescent protein transgenic rats

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Neural Regeneration Research 2013年第2期8卷 162-168页

作者： Haogang Xue Chunying Yang Xiaodong Ge Weiqi Sun Chun Li Mingyu Qi Department of Orthopedic Surgery First Clinical Hospital Beihua University

Kisspeptin is essential for activation of the hypothalamo-pituitary-gonadal axis. In this study, we established gonadotropin-releasing hormone/enhanced green fluorescent protein transgenic rats. Rats were injected with 1, 10, or 100 pM kisspeptin-10, a peptide derived from full-length kisspeptin, into the arcuate nucleus and medial preoptic area, and with the kJsspeptJn antagonist peptJde 234 into the lateral cerebral ventricle. The results of immunohistochemical staining revealed that pulsatile luteinizing hormone secretion was suppressed after injection of antagonist peptide 234 into the lateral cerebral ventricle, and a significant increase in luteinizing hormone level was observed after kisspeptin-10 injection into the arcuate nucleus and medial preoptic area. The results of an enzyme-linked immunosorbent assay showed that luteinizing hormone levels during the first hour of kisspeptin-10 infusion into the arcuate nucleus were significantly greater in the 100 pM kisspeptin-10 group than in the 10 pM kisspeptin-10 group. These findings indicate that kisspeptin directly promotes gonadotropin-releasing hormone secretion and luteinizing hormone release in gonadotropin-releasing hormone/enhanced green fluorescent protein transgenic rats. The arcuate nucleus is a key component of the kisspeptin-G protein-coupled receptor 54 signaling pathway underlying regulating luteinizing hormone pulse secretion.

关键词： neural regeneration basic research gonadotropin-releasing hormone enhanced green fluorescentprotein transgenic luteinizing hormone G protein-coupled receptor 54 medial preoptic area arcuate nucleus anteroventral periventricular nucleus organum vasculosum of the laminaterminalis photographs-containing paper neuroregeneration

Neuropeptide Y and leptin receptor expression in the hypothalamus of rats with chronic immobilization stress

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Neural Regeneration Research 2013年第18期8卷 1721-1726页

作者： Shaoxian Wang Jiaxu Chen Guangxin Yue Minghua Bai Meijing Kou Zhongye Jin School of Pre-clinical Medicine Beijing University of Chinese Medicine Traditional Chinese Medicine College of Hebei Medical University Institute of Basic Theory in Chinese Medicine China Academy of Chinese Medical Sciences

In this study, Sprague-Dawley rats were immobilized to a frame for 3 hours a day for 21 days to establish a model of chronic immobilization stress. The body weight and food intake of rats subjected to chronic immobilization stress were significantly decreased compared with the control group. Dual-labeling immunofluorescence revealed that the expression of leptin receptor and the co-localization coeffient in these leptic receptor neurons in the arcuate nucleus of the hypothalamus were both upregulated, while the number of neuropeptide Y neurons was decreased. Chronic immobilization stress induced high expression of leptin receptor in the arcuate nucleus and suppressed the synthesis and secretion of neuropeptide Y, thereby disrupting the pathways in the arcuate nucleus that regulate feeding behavior, resulting in diminished food intake and reduced body weight.

关键词： neural regeneration chronic immobilization stress hypothalamus arcuate nucleus doubleimmunofluorescence neuropeptide Y leptin receptor feeding center body weight grants-supported paper neuroregeneration