ADENOSINE REDUCES CORTICAL NEURONAL INJURY INDUCED BY OXYGEN OR GLUCOSE DEPRIVATION INVITRO
ADENOSINE REDUCES CORTICAL NEURONAL INJURY INDUCED BY OXYGEN OR GLUCOSE DEPRIVATION INVITRO
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DOI：
10.1016/0304-3940(88)90547-2
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发表时间：
1988-07-08
影响因子：
2.5
通讯作者：
CHOI, DW
中科院分区：
文献类型：
--
作者：
GOLDBERG, MP;MONYER, H;CHOI, DW
内源性神经调节嘌呤，腺苷，当加入到严重缺乏氧气或葡萄糖的分离的皮质细胞培养中时，实质上减轻了神经元的退化。腺苷的保护作用在30~1000µm之间呈浓度依赖性(EC50约为100µm)，并可被稳定的腺苷类似物N6-环己基腺苷(10µm)所模拟。与突触后谷氨酸受体拮抗剂不同，腺苷不能改变外源性谷氨酸的神经毒性，突触后谷氨酸受体拮抗剂也可以阻断这些形式的神经元损伤。
The endogenous neuromodulatory purine, adenosine, substantially attenuated neuronal degeneration when added to dissociated cortical cell cultures acutely deprived of either oxygen or glucose. The protective effect of adenosine was concentration-dependent between 30 and 1000 .mu.M (EC50 about 100 .mu.M), and could be mimicked by the stable adenosine analogue N6-cyclohexyladenosine (10 .mu.M). Unlike postsynaptic glutamate receptor antagonists, which also block these forms of neuronal injury, adenosine did not alter the neurotoxicity of exogenously applied glutamate.