desipramine inhibits histamine h1 receptor-induced ca2+ signaling in rat hypothalamic cells去郁敏抑制组胺h1 receptor-induced在老鼠的下丘脑细胞钙离子信号.pdfVIP
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desipramineinhibitshistamineh1receptor-inducedca2signalinginrathypothalamiccells去郁敏抑制组胺h1receptor-induced在老鼠的下丘脑细胞钙离子信号
Desipramine Inhibits Histamine H1 Receptor-Induced Ca2+ Signaling in Rat Hypothalamic Cells 1. 1. 2 1 1 3 2 Ji-Ah Kang , Keimin Lee , Kwang Min Lee , Sukhee Cho , Jinsoo Seo , Eun-Mi Hur , Chul-Seung Park , 4 1 Ja-Hyun Baik , Se-Young Choi * 1 Department of Physiology, Dental Research Institute, Seoul National University School of Dentistry, Seoul Republic of Korea, 2 School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea, 3 Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America, 4 School of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea Abstract The hypothalamus in the brain is the main center for appetite control and integrates signals from adipose tissue and the gastrointestinal tract. Antidepressants are known to modulate the activities of hypothalamic neurons and affect food intake, but the cellular and molecular mechanisms by which antidepressants modulate hypothalamic function remain unclear. Here we have investigated how hypothalamic neurons respond to treatment with antidepressants, including desipramine and sibutramine. In primary cultured rat hypothalamic cells, desipramine markedly suppressed the elevation of intracellular Ca2+ evoked by histamine H1 receptor activation. Desipramine also inhibited the histamine-induced Ca2+ increase and the expression of corticotrophin-releasing hormone in hypothalamic GT1-1 cells. The effect of desipramine was not affected by pretreatment with prazosin or propranolol, excluding catecholamine reuptake activity of desipramine as an underlying mec
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