Lysophosphatidic acid stimulates calcium transients in enteric glia

被引：21

作者：

Segura, BJ ^{[1
]}

Zhang, W ^{[1
]}

Cowles, RA ^{[1
]}

Xiao, L ^{[1
]}

Lin, TR ^{[1
]}

Logsdon, C ^{[1
]}

Mulholland, MW ^{[1
]}

机构：

[1] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA

来源：

NEUROSCIENCE | 2004年 / 123卷 / 03期

关键词：

enteric nervous system; sphingolipid; EDG receptors;

D O I：

10.1016/j.neuroscience.2003.10.003

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The enteric nervous system plays an integral role in the gastrointestinal tract. Within this intricate network, enteric glia are crucial in the maintenance of normal bowel function, yet their signaling mechanisms are poorly understood. Enteric glia, and not enteric neurons, selectively responded to lysophosphatidic acid (LPA), a product of phosphatidylcholine metabolism, with dose-dependent calcium (Ca2+) signaling over a range from 100 pM to 10 muM. The elicited calcium transients involved both the mobilization of intracellular Ca2+ stores and the influx of extracellular Ca2+ as LPA signals were obliterated following the depletion of intracellular Ca2+ and attenuated by the removal of Ca2+ from the perfusion buffer. Pretreatment with pertussis toxin (100 ng/ml) reduced the magnitude of LPA Ca2+ transients (95 +/- 20 nM vs 168 +/- 17 nM for controls). Repetitive exposure yielded diminished responsiveness, with a 25% reduction in [Ca2+](i) between first and second exposures. Inhibition of the inositol 1,4,5-trisphosphate (IP3) receptor with 200 muM 2-aminoethoxydiphenylborate (2APB) abolished LPA signals. RT-PCR analysis demonstrated the presence of two LPA-coupled endothelial differentiation gene (EDG) receptor mRNAs (EDG-2 and EDG-7) in myenteric plexus primary cultures. EDG-2 expression in glial cells of the ENS was confirmed immunocytochemically. (C) 2003 IBRO. Published by Elsevier Ltd. All rights reserved.

引用

页码：687 / 693

页数：7

共 20 条

[1] Recombinant human G protein-coupled lysophosphatidic acid receptors mediate intracellular calcium mobilization [J].