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培养的大鼠皮质神经元中温度依赖性N-甲基-D-天冬氨酸受体介导的细胞毒性

Temperature-dependent N-methyl-D-aspartate receptor-mediated cytotoxicity in cultured rat cortical neurons.

作者信息

Takadera Tsuneo, Ohyashiki Takao

机构信息

Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa 920-1148, Japan.

出版信息

Neurosci Lett. 2007 Aug 9;423(1):24-8. doi: 10.1016/j.neulet.2007.06.033. Epub 2007 Jun 29.

Abstract

Hypothermia protects against hypoxic or ischemic damage. However, the mechanisms by which brain cooling prevents hypoxic or ischemic damage are not clear. We examined whether hypothermia protects against excitotoxicity in cultured cortical cells. Exposure of cortical cell culture to 500 microM N-methyl-D-aspartate (NMDA) for 15 min at 32 degrees C or 37 degrees C did not induce neurotoxicity. On the other hand, reduction of temperature to 20 degrees C resulted in widespread neuronal disintegration by the following day. Moreover, intracellular calcium concentration increased markedly by adding NMDA to cells at 20 degrees C. These results suggest that profound hypothermia does not protect neurons from excitotoxicity by inhibiting NMDA receptor activity.

摘要

体温过低可预防缺氧或缺血性损伤。然而,脑部降温预防缺氧或缺血性损伤的机制尚不清楚。我们研究了体温过低是否能保护培养的皮质细胞免受兴奋性毒性作用。在32℃或37℃下,将皮质细胞培养物暴露于500微摩尔/升的N-甲基-D-天冬氨酸(NMDA)中15分钟不会诱导神经毒性。另一方面,将温度降至20℃会导致第二天广泛的神经元解体。此外,在20℃下向细胞中添加NMDA会使细胞内钙浓度显著增加。这些结果表明,深度体温过低并不能通过抑制NMDA受体活性来保护神经元免受兴奋性毒性作用。

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