Department of Neurology, The First Affiliated Hospital in Harbin Medical University, 37 Yiyuan Street, Harbin, Heilongjiang, 150001, People's Republic of China.
Neurol Sci. 2013 Jul;34(7):1189-95. doi: 10.1007/s10072-012-1220-9. Epub 2012 Oct 31.
Ischemic brain cell death is presumably caused by excitotoxicity. In addition to an increase of glutamate release during ischemia, the deficiency of astrocytic glutamate-reuptake may cause glutamate accumulation, which results in GABAergic neurons being vulnerable to ischemia. To confirm this hypothesis, we studied the pathophysiological changes of cortical astrocytes and GABAergic neurons during ischemia as well as the prevention of their injuries. Ischemia led to the sequential impairments of astrocytic glutamate-transporter currents and GABAergic neuronal excitability. The changes were partially reversed by 3,5-DHPG, an agonist of type-I/V metabotropic glutamate receptors (mGluR). Thus, mGluR₁,₅ activation may be useful against the sequential impairment of cortical astrocytes and GABAergic neurons in an early stage of ischemia.
缺血性脑细胞死亡推测是由兴奋性毒性引起的。除了在缺血期间谷氨酸释放增加之外，星形胶质细胞谷氨酸摄取的不足可能导致谷氨酸积累，从而使 GABA 能神经元容易受到缺血的影响。为了证实这一假说，我们研究了缺血期间皮质星形胶质细胞和 GABA 能神经元的病理生理变化以及它们损伤的预防。缺血导致星形胶质细胞谷氨酸转运体电流和 GABA 能神经元兴奋性的顺序损伤。这些变化部分被 3,5-DHPG 逆转，3,5-DHPG 是 I/V 型代谢型谷氨酸受体 (mGluR) 的激动剂。因此，mGluR₁,₅的激活可能对抗缺血早期皮质星形胶质细胞和 GABA 能神经元的顺序损伤有用。
