کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6281541 | 1615115 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Gintonin, a novel ginseng-derived lysophosphatidic acid receptor ligand, stimulates neurotransmitter release
ترجمه فارسی عنوان
گینتونین، لیگاند گیرنده اسید لیسوفسفیدید اسید ریشه ای جینسنگ، باعث تحریک انتشار عصبی می شود
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کلمات کلیدی
GPCRPC12[Ca2+]i transient[Ca2+]i - [Ca2 +] ineurotransmitter release - انتشار نوروترانسمیترGinseng - جینسنگDopamine - دوپامینintracellular calcium concentration - غلظت کلسیم داخل سلولیLPA receptor - گیرنده LPAlysophosphatidic acid receptor - گیرنده اسید لیسوفسفیدیدG protein-coupled receptor - گیرندههای جفتشونده با پروتئین جیGintonin - گینتونین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Gintonin is a novel ginseng-derived G protein-coupled lysophosphatidic acid (LPA) receptor ligand. Gintonin elicits an intracellular calcium concentration [Ca2+]i transient via activation of LPA receptors and regulates calcium-dependent ion channels and receptors. [Ca2+]i elevation by neurotransmitters or depolarization is usually coupled to neurotransmitter release in neuronal cells. Little is known about whether gintonin-mediated [Ca2+]i transients are also coupled to neurotransmitter release. The PC12 cell line is derived from a pheochromocytoma of the rat adrenal medulla and is widely used as a model for catecholamine release. In the present study, we examined the effects of gintonin on dopamine release in PC12 cells. Application of gintonin to PC12 cells induced [Ca2+]i transients in concentration-dependent and reversible manners. However, ginsenoside Rg3, another active ingredient of ginseng, induced a lagged and irreversible [Ca2+]i increase. The induction of gintonin-mediated [Ca2+]i transients was attenuated or blocked by the LPA1/3 receptor antagonist Ki16425, a phospholipase C inhibitor, an inositol 1,4,5-triphosphate receptor antagonist, and an intracellular Ca2+ chelator. Repeated treatment with gintonin induced homologous desensitization of [Ca2+]i transients. Gintonin treatment in PC12 cells increased the release of dopamine in a concentration-dependent manner. Intraperitoneal administration of gintonin to mice also increased serum dopamine concentrations. The present study shows that gintonin-mediated [Ca2+]i transients are coupled to dopamine release via LPA receptor activation. Finally, gintonin-mediated [Ca2+]i transients and dopamine release via LPA receptor activation might explain one mechanism of gintonin-mediated inter-neuronal modulation in the nervous system.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 584, 1 January 2015, Pages 356-361
Journal: Neuroscience Letters - Volume 584, 1 January 2015, Pages 356-361
نویسندگان
Sung-Hee Hwang, Byung-Hwan Lee, Sun-Hye Choi, Hyeon-Joong Kim, Seok-Won Jung, Hyun-Sook Kim, Ho-Chul Shin, Hyun Jin Park, Keun Hong Park, Myung Koo Lee, Seung-Yeol Nah,