Gintonin, a novel ginseng-derived lysophosphatidic acid receptor ligand, stimulates neurotransmitter release
- Authors
- Hwang, Sung-Hee; Lee, Byung-Hwan; Choi, Sun-Hye; Kim, Hyeon-Joong; Jung, Seok-Won; Kim, Hyun-Sook; Shin, Ho-Chul; Park, Hyun Jin; Park, Keun Hong; Lee, Myung Koo; Nah, Seung-Yeol
- Issue Date
- Jan-2015
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- GinsengGintoninLPA receptor[Ca2+](i) transientDopamineNeurotransmitter release
- Citation
- NEUROSCIENCE LETTERS, v.584, pp.356 - 361
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEUROSCIENCE LETTERS
- Volume
- 584
- Start Page
- 356
- End Page
- 361
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/158027
- DOI
- 10.1016/j.neulet.2014.11.007
- ISSN
- 0304-3940
- Abstract
- 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 Rg(3), 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.
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