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N-甲基-D-天冬氨酸受体介导的来自p53基因敲除的永生化小鼠神经干细胞分化的神经元中的Ca2+反应。

NMDA receptor mediated Ca2+ responses in neurons differentiated from p53-/- immortalized Murine neural stem cells.

作者信息

Yamada K, Hisatsune T, Uchino S, Nakamura T, Kudo Y, Kaminogawa S

机构信息

Department of Applied Biological Chemistry, University of Tokyo, Japan.

出版信息

Neurosci Lett. 1999 Apr 2;264(1-3):165-7. doi: 10.1016/s0304-3940(99)00134-2.

DOI:10.1016/s0304-3940(99)00134-2
PMID:10320040
Abstract

NMDA receptors play important roles in brain formation by taking part in synaptogenesis and apoptosis. In the present study, the expression of NMDA receptors was analyzed in a neural stem cell line, MSP-1, which lacks p53. p53 is a transcription factor involved in excitotoxic neuronal apoptosis. It is quite likely that p53-mediated transcription control affects the expression of NMDA receptors inducing intracellular Ca2+ signaling after neuronal differentiation and is essential for neural development. By means of calcium digital imaging, NMDA receptor-mediated Ca2+ responses were detected from cultured neurons differentiated from neural stem cells which lack p53. This result implies that p53-related apoptosis is not due to NMDA receptor expression.

摘要

N-甲基-D-天冬氨酸(NMDA)受体通过参与突触形成和细胞凋亡在大脑形成过程中发挥重要作用。在本研究中,对缺乏p53的神经干细胞系MSP-1中NMDA受体的表达进行了分析。p53是一种参与兴奋性毒性神经元凋亡的转录因子。很可能p53介导的转录调控会影响NMDA受体的表达,在神经元分化后诱导细胞内Ca2+信号传导,并且对神经发育至关重要。通过钙数字成像,从缺乏p53的神经干细胞分化而来的培养神经元中检测到了NMDA受体介导的Ca2+反应。这一结果表明,p53相关的细胞凋亡并非由NMDA受体表达所致。

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Glutamate triggers elevation of intracellular Ca(2+) concentration in neural precursor cells.谷氨酸会引发神经前体细胞内钙离子浓度的升高。
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