The effect of bradykinin on the electrical activity of rat myenteric neurons.

The effect of bradykinin on the electrical activity of rat myenteric neurons.
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缓激肽对大鼠肌间神经元电活动的影响

DOI:
10.1016/j.ejphar.2014.05.020
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发表时间:
2014
影响因子:
5
通讯作者:
Diener M
Diener M
中科院分区:
医学2区
文献类型:
--
作者:
Würner L;Pouokam E;Diener M

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缓激肽是一种参与肠道炎症过程的介质。在这里,我们研究了缓激肽对大鼠肌间神经元电活动的影响,这是调节胃肠运动的关键因素。微电极阵列测得缓激肽(2×10−8mol/L)引起双相动作电位频率增加。胞浆内钙离子浓度([Ca~(2+)]i)呈双相升高,在约40%的肌间神经元中观察到这种升高。缓激肽B1受体激动剂Des-arg9-Bradykinin和缓激肽B2受体激动剂hi3-bradykinin对[Ca~(2+)]i的作用相似。免疫细胞化学染色证实肌间神经节细胞表达这两种受体。实时荧光定量聚合酶链式反应显示,细胞培养过程中可诱导的B1受体表达上调。吡罗昔康对环氧合酶的抑制可减弱缓激肽对肌间神经元电活动的影响。微电极阵列对胶质细胞生长的抑制不影响缓激肽引起的动作电位频率的改变。这表明,可能介导缓激肽作用的前列腺素并不是由神经胶质细胞独有释放的。缓激肽诱导的细胞外钙升高依赖于细胞外钙离子的存在,并被电压依赖性钙通道阻断剂Co2+、CD2+和Ni2+所抑制,表明激动素刺激细胞外钙内流。因此,缓激肽通过质膜上的钙通道诱导肌间神经元内钙内流。
Bradykinin is a mediator involved in inflammatory processes in the gut. Here we investigated the effect of bradykinin on the electrical activity of rat myenteric neurons, the key players for regulation of gastrointestinal motility. Bradykinin (2×10−8mol/l) induced a biphasic increase in frequency of action potentials measured with microelectrode arrays. This increase was mirrored by a biphasic increase in cytosolic Ca2+concentration ([Ca2+]i), which was observed in about 40% of the myenteric neurons. The bradykinin B1receptor agonist des-arg9-bradykinin as well as the bradykinin B2receptor agonist hyp3-bradykinin induced a similar effect on [Ca2+]i. Immunocytochemical stainings confirmed the expression of both receptor types by myenteric ganglionic cells. Real time PCR showed that the inducible B1receptor was upregulated during cell culture. The inhibition of cyclooxygenases with piroxicam reduced the effect of bradykinin on the electrical activity of myenteric neurons. The suppression of the glial growth on microelectrode arrays did not affect the bradykinin-induced change in frequency of action potentials. This suggests that prostaglandins, which probably mediate the effect of bradykinin, are not exclusively released from glial cells.The bradykinin-induced increase in [Ca2+]iwas dependent on the presence of extracellular Ca2+and was inhibited by Co2+, Cd2+, and Ni2+, blockers of voltage-dependent Ca2+channels, indicating a stimulation of the influx of extracellular Ca2+by the kinin. Consequently, bradykinin induces a Ca2+influx in myenteric neurons via Ca2+channels in the plasma membrane.
地塞米松和蛋白激酶 C 抑制剂对离体大鼠回肠中缓激肽 B1 mRNA 诱导和缓激肽 B1 受体介导的收缩反应的影响。
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DOI: 10.1016/j.ejphar.2012.02.001
发表时间: 2012
影响因子: 5
作者:
Rehn M;Diener M
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大鼠结肠上皮缓激肽 B1 受体的诱导
DOI: --
发表时间: 1997
影响因子: 7.3
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神经系统疾病中的胃肠功能障碍:跨学科国际研讨会报告
DOI: --
发表时间: 1994
期刊:
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通讯作者: R. Pfeiffer