Effects of axonal injury on ganglion cell survival and glutamate homeostasis
Effects of axonal injury on ganglion cell survival and glutamate homeostasis
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DOI：
10.1016/s0361-9230(03)00075-3
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发表时间：
2004-02-15
影响因子：
3.8
通讯作者：
Dreyer, EB
中科院分区：
文献类型：
--
作者：
Vorwerk, CK;Zurakowski, D;Dreyer, EB
轴突损伤导致一系列病理事件，最终导致神经元死亡。视神经夹伤可用于探讨创伤性中枢神经系统功能障碍的组织学和分子变化。虽然视神经损伤后视网膜神经节细胞死亡的确切机制尚未阐明，但谷氨酸拮抗剂可以保护视神经切断后的视网膜神经节细胞。因此，我们评估视神经挤压对细胞外谷氨酸水平的影响。在Long-Evans大鼠视神经挤压后1至28天评估神经节细胞存活和细胞外谷氨酸水平。视神经挤压导致细胞外谷氨酸的上升，这种上升被阻断治疗与美金刚，利鲁唑，尼莫地平。部分视神经挤压导致玻璃体谷氨酸增加，可能是通过细胞内内容物的释放。这种释放的谷氨酸可以导致额外的神经节细胞损失。未来的工作将有助于进一步阐明轴突切断术诱导神经节细胞兴奋性毒性损伤的步骤，并可能表明保护性干预措施。(C)2003年爱思唯尔科学公司All rights reserved.
Axonal trauma leads to a series of pathologic events that can culminate in neuronal death. Optic nerve crush can be used to explore histologic and molecular changes in traumatic central nervous system malfunction. Although the precise mechanisms of retinal ganglion cell death after optic nerve crush have not been elucidated, glutamate antagonists can protect retinal ganglion cells after axotomy. We, therefore, evaluated the effect of optic nerve crush on levels of extracellular glutamate. Ganglion cell survival and extracellular glutamate levels were assessed from 1 to 28 days after optic nerve crush in Long-Evans rats. Optic nerve crush led to a rise in extracellular glutamate; this rise was blocked by treatment with memantine, riluzole, and nimodipine. Partial optic nerve crush leads to an increase in vitreal glutamate, perhaps through release of intracellular contents. This released glutamate can contribute to additional ganglion cell loss. Future work will help to additionally unravel the steps by which axotomy induces excitotoxic damage to ganglion cells, and perhaps indicate protective interventions. (C) 2003 Elsevier Science Inc. All rights reserved.