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碱性成纤维细胞生长因子可保护原代培养的小脑神经元免受N-甲基-D-天冬氨酸(NMDA)和非NMDA受体介导的神经毒性作用。

Basic fibroblast growth factor protects cerebellar neurons in primary culture from NMDA and non-NMDA receptor mediated neurotoxicity.

作者信息

Fernández-Sánchez M T, Novelli A

机构信息

Department of Functional Biology, School of Medicine, University of Oviedo, Spain.

出版信息

FEBS Lett. 1993 Nov 29;335(1):124-31. doi: 10.1016/0014-5793(93)80453-2.

Abstract

We have investigated the ability of bFGF to protect cerebellar neurons from neurotoxicity by excitatory amino acids. We have found that preincubation with 1-2.5 nM bFGF for 1-6 days significantly protected neurons from excitotoxic damage via NMDA receptors as well as ionotropic non-NMDA receptors. bFGF neuroprotection appeared not to be dependent upon neuronal differentiation and was not mimicked by other neurotrophins including BDNF, NT-3 and NGF. A greater rise in extracellular calcium-dependent cGMP formation, following either depolarization or excitatory amino acid receptor activation was observed in bFGF-pretreated neurons. We suggest that neuroprotection from excitotoxicity following bFGF treatment may be associated to the modulation of neurochemical pathways dependent upon extracellular calcium influx.

摘要

我们研究了碱性成纤维细胞生长因子(bFGF)保护小脑神经元免受兴奋性氨基酸所致神经毒性的能力。我们发现,用1 - 2.5 nM的bFGF预孵育1 - 6天,可通过N-甲基-D-天冬氨酸(NMDA)受体以及离子型非NMDA受体显著保护神经元免受兴奋性毒性损伤。bFGF的神经保护作用似乎不依赖于神经元分化,并且其他神经营养因子(包括脑源性神经营养因子(BDNF)、神经营养因子-3(NT-3)和神经生长因子(NGF))无法模拟这种作用。在bFGF预处理的神经元中,无论是去极化还是兴奋性氨基酸受体激活后,细胞外钙依赖性环磷酸鸟苷(cGMP)形成的升高幅度都更大。我们认为,bFGF治疗后对兴奋性毒性的神经保护作用可能与依赖细胞外钙内流的神经化学途径的调节有关。

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