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缺氧可预防海藻酸的神经毒性。

Hypoxia protects against the neurotoxicity of kainic acid.

作者信息

Pohle W, Rauca C

机构信息

Department of Pharmacology and Toxicology, Medical Faculty of the Otto-v.-Guericke-University Magdeburg, FRG.

出版信息

Brain Res. 1994 May 2;644(2):297-304. doi: 10.1016/0006-8993(94)91693-4.

Abstract

A normobar hypoxia (9% oxygen) of 8 h reduces the neurotoxicity of a subcutaneous injection of 10 mg/kg kainic acid given one week later. Both seizures and degenerative changes, including cell death of hippocampal and cortical neurons are markedly decreased by hypoxia. It is also shown that hypoxia also markedly reduced the extensive depletion of zinc from mossy fiber terminals normally induced by kainic acid. This suggests that a protective mechanism induced by hypoxia may affect the glutamatergic transmission in these synapses and prevent excessive synaptic excitation. The possible involvement of adenosine and/or GABA in this protective mechanism is discussed.

摘要

8小时的常压缺氧(9%氧气)可降低一周后皮下注射10mg/kg海藻酸的神经毒性。缺氧可显著减少癫痫发作和退行性变化,包括海马体和皮层神经元的细胞死亡。研究还表明,缺氧也显著减少了通常由海藻酸诱导的苔藓纤维终末锌的大量消耗。这表明缺氧诱导的保护机制可能影响这些突触中的谷氨酸能传递,并防止过度的突触兴奋。文中讨论了腺苷和/或GABA可能参与这种保护机制。

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