Involvement of prostaglandin E2 derived from enteric glial cells in the action of bradykinin in cultured rat myenteric neurons
Involvement of prostaglandin E2 derived from enteric glial cells in the action of bradykinin in cultured rat myenteric neurons
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DOI：
10.1016/j.neuroscience.2006.12.052
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发表时间：
2007-03
期刊：
影响因子：
3.3
通讯作者：
M. Murakami;T. Ohta;K. Otsuguro;S. Ito
中科院分区：
文献类型：
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作者：
M. Murakami;T. Ohta;K. Otsuguro;S. Ito
我们分别利用fura-2和全细胞膜片钳技术的比例Ca2+成像技术，表征了缓激肽（BK）诱导的细胞内Ca2+浓度（[Ca2+]i）和培养大鼠肌间神经元膜电位的变化。BK引起了[Ca2+]i的剂量依赖性增加，这种增加被B2受体拮抗剂HOE 140所消除，但被B1受体拮抗剂[Lys-des-Arg9]-BK所消除。[Lys-des-Arg9]-HOE140，一种B1受体激动剂，未能引起[Ca2+]i反应。B2受体抗体与PGP9.5或S100双染色表明B2受体在神经元和神经胶质细胞中表达。bk引起的[Ca2+]i升高被吲哚美辛（一种非选择性环氧化酶（COX）抑制剂）抑制，并被前列腺素E2（PGE2）增强。BK增加了培养的肌丛细胞中pge2的释放，在高密度培养时，BK诱导神经元中[Ca2+]i的大量增加，而在低密度培养时，BK诱导神经元中[Ca2+]i的少量增加，而在抑制肠胶质细胞增殖时，BK诱导神经元中[Ca2+]i的少量增加。BK引起肌肠神经元缓慢而持续的去极化，对吲哚美辛敏感。这些结果表明，BK通过激活B2受体导致大鼠肌间神经细胞的[Ca2+]i增加和去极化，这与神经细胞响应BK释放pge2有关，提示BK在大鼠肌间神经丛中的作用可能与神经-胶质相互作用有关。
We characterized bradykinin (BK)-induced changes in the intracellular Ca2+concentration ([Ca2+]i) and membrane potential in cultured rat myenteric neurons using ratiometric Ca2+imaging with fura-2 and the whole-cell patch-clamp technique, respectively. BK evoked a dose-dependent increase of [Ca2+]i that was abolished by HOE 140, a B2 receptor antagonist but not by [Lys-des-Arg9]-BK, a B1 receptor antagonist. [Lys-des-Arg9]-HOE140, a B1 receptor agonist, failed to cause a [Ca2+]i response. Double staining with antibodies against the B2 receptor together with PGP9.5 or S100 indicated that B2 receptors were expressed in neurons and glial cells. The BK-evoked [Ca2+]i increase was suppressed by indomethacin, a non-selective cyclooxygenase (COX) inhibitor, and potentiated by prostaglandin E2(PGE2). The release of PGE2from cultured myenteric plexus cells was increased by BK. BK induced a large increase in [Ca2+]i in neurons when myenteric plexus cells were cultured at the high density but not at the low density, and caused a small increase in [Ca2+]i in neurons when proliferation of enteric glial cells was suppressed. BK evoked a slow and sustained depolarization in myenteric neurons, which was sensitive to indomethacin. These results indicated that BK caused a [Ca2+]i increase and depolarization in rat myenteric neurons through the activation of B2 receptors, which was partly associated with PGE2released from glial cells in response to BK. It is suggested that a neuron–glial interaction plays an important role in the effect of BK in the rat myenteric plexus.