Inability of volatile anesthetics to inhibit oxygen-glucose deprivation-induced glutamate release via glutamate transporters and anion channels in rat corticostriatal slices
Inability of volatile anesthetics to inhibit oxygen-glucose deprivation-induced glutamate release via glutamate transporters and anion channels in rat corticostriatal slices
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DOI：
10.1016/j.brainres.2008.06.063
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发表时间：
2008-08-28
期刊：
影响因子：
2.9
通讯作者：
Zuo, Zhiyi
中科院分区：
文献类型：
--
作者：
Jung, Hae-Hyuk;Lee, Jeong Jin;Zuo, Zhiyi
缺血诱导的细胞外谷氨酸蓄积和随后的兴奋性毒性是导致缺血性脑损伤的重要因素。挥发性麻醉剂已被证明可以减少缺血性脑损伤。在这里，我们证明了氧-葡萄糖剥夺(OGD，模拟体外缺血)增加了成年大鼠皮质纹状体脑片细胞外谷氨酸的积累。谷氨酸转运体2型抑制剂二氢激动酸和容量激活阴离子通道阻断剂4，4‘-二硝基二苯乙烯-2，2’-二磺酸可减少这种增加的蓄积。临床相关浓度的异氟醚、七氟醚和地氟醚不影响OGD诱导的成年大鼠脑片细胞外谷氨酸蓄积。异氟醚也不改变OGD诱导的新生/幼年大鼠脑片细胞外谷氨酸蓄积。这些结果表明，OGD诱导的谷氨酸蓄积通过谷氨酸转运体和容量激活的阴离子通道参与谷氨酸的反向转运。挥发性麻醉剂可能不会抑制这种细胞外谷氨酸的积累。(C)2008爱思唯尔B.V.保留所有权利。
Ischemia-induced extracellular glutamate accumulation and the subsequent excitotoxicity contribute significantly to ischemic brain injury. Volatile anesthetics have been shown to reduce ischemic brain injury. Here, we showed that oxygen-glucose deprivation (OGD, to simulate ischemia in vitro) increased extracellular glutamate accumulation in the corticostriatal slices of adult rats. This increased accumulation was reduced by dihydrokinate, a glutamate transporter type 2 inhibitor, and 4,4'-dinitrostilbene-2,2'-disulfonic acid, a blocker for volume-activated anion channels. The volatile anesthetics isoflurane, sevoflurane and desflurane at clinically relevant concentrations did not affect the OGD-incluced extracellular glutamate accumulation from brain slices of adult rats. Isoflurane also did not change the OGD-induced extracellular glutamate accumulation from brain slices of newborn/young rats. These results suggest that the OGD-induced glutamate accumulation involves reversed transport of glutamate via glutamate transporters and volume-activated anion channels. Volatile anesthetics may not inhibit this extracellular glutamate accumulation. (C) 2008 Elsevier B.V. All rights reserved.