Cui Y, Zhang L, Utsunomiya K, Yanase H, Mitani A, Kataoka K
Department of Physiology, School of Medicine, Ehime University, Onsen-gun, Japan.
Neurosci Lett. 1999 Aug 27;271(3):191-4. doi: 10.1016/s0304-3940(99)00556-x.
The levels of extracellular glutamate were measured in the dentate gyrus by using an in vivo brain microdialysis method to determine whether the ischemia-induced glutamate release might be correlated with the neuronal vulnerability to ischemia. A microdialysis membrane was placed in CA4 (vulnerable to ischemia) and the molecular and granule cell layers of the dentate gyrus (resistant to ischemia) of gerbils. A significant increase in glutamate levels was induced in the normal dentate gyrus during 10-min ischemia. The increase was completely suppressed during the first 5 min of ischemia when CA4 neurons were eliminated. Thus, it was indicated that during the first 5 min of ischemia glutamate was released mostly from CA4 neurons but not from granule cells of the dentate gyrus. During the second half of 10-min ischemia, a significant increase in glutamate release was induced even in the dentate gyrus where CA4 neurons were eliminated; this increase was significantly suppressed by inhibiting proliferation of astrocytes. A large part of glutamate that was released during the second half of 10-min ischemia was considered to be attributable to glutamate release from astrocytes.
采用活体脑微透析法测定齿状回细胞外谷氨酸水平，以确定缺血诱导的谷氨酸释放是否可能与神经元对缺血的易损性相关。将微透析膜置于沙鼠的CA4区（对缺血敏感）以及齿状回的分子层和颗粒细胞层（对缺血有抗性）。在10分钟缺血期间，正常齿状回中的谷氨酸水平显著升高。当CA4神经元在缺血的前5分钟被消除时，这种升高被完全抑制。因此，表明在缺血的前5分钟，谷氨酸主要从CA4神经元释放，而不是从齿状回的颗粒细胞释放。在10分钟缺血的后半段，即使在CA4神经元被消除的齿状回中，谷氨酸释放也显著增加；通过抑制星形胶质细胞增殖，这种增加被显著抑制。在10分钟缺血后半段释放的大部分谷氨酸被认为归因于星形胶质细胞释放的谷氨酸。
