Transient in vivo membrane depolarization and glutamate release before anoxic depolarization in rat striatum
Transient in vivo membrane depolarization and glutamate release before anoxic depolarization in rat striatum
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DOI：
10.1016/s0006-8993(99)01481-x
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发表时间：
1999-06-12
期刊：
影响因子：
2.9
通讯作者：
Ishikawa, K
中科院分区：
文献类型：
--
作者：
Kunimatsu, T;Asai, S;Ishikawa, K
在脑缺血、缺氧或低氧条件下，细胞外谷氨酸（[GLU]e）增加已被认为与神经元细胞损伤和死亡有关。我们进行实时监测[GLU]e动态在体内大鼠纹状体在全身急性缺氧或缺氧，以及监测直流电位（DC）和脑血流量（CBF）。成年Wistar大鼠经口气管插管，人工呼吸室内空气。然后植入微透析电极、温度传感器探针、直流微电极和激光多普勒探针。吸入气体改为100%N-2（缺氧）或3、5或8%O-2（其余为N-2）（缺氧）。100% N-2时，观察到明显的双相[GLU]e升高。在3%O-2条件下，在缺氧去极化（AD）之前，[GLU]e出现短暂增加。但氧气含量只有5%。短暂[GLU]e增加的开始明显延迟。缺氧诱导的去极化开始于约100 s。3%O-2诱导的短暂去极化和AD几乎与[GLU]e的短暂和AD诱导的增加同时开始。同样，对5%O-2的反应显示短暂去极化和AD诱导的[GLU]e增加的显著延迟。在3或5%O-2低氧损伤期间，CBF始终保持在对照水平以上，即，在心脏骤停之前。我们的新的透析电极方法采用GOX和二茂铁结合的牛血清白蛋白允许在严重缺氧的早期阶段在体内短暂的[GLU]e动力学评价。(C)1999 Elsevier Science B. V.保留所有权利。
Increased extracellular glutamate ([GLU]e), under the condition of cerebral ischemia, anoxia or hypoxia, has been recognized as being associated with neuronal cell damage and death. We performed real-time monitoring of [GLU]e dynamics in vivo in the rat striatum during systemic acute anoxia or hypoxia, as well as monitoring the direct current potential (DC) and cerebral blood flow (CBF). Adult Wistar rats were orotracheally intubated and artificially ventilated with room air. A microdialysis electrode, temperature sensor probe, DC microelectrode and laser Doppler probe were then implanted. The inspired gas was changed to 100% N-2 (anoxia), or to 3, 5 or 8% O-2 (remainder N-2) (hypoxia). With 100% N-2, distinct biphasic [GLU]e elevations were observed. With 3% O-2, a transient [GLU]e increase was seen before anoxic depolarization (AD). With 5% O-2, however. the start of the transient [GLU]e increase was significantly delayed. Anoxia-induced depolarization started at about 100 s. The 3% O-2-induced transient depolarization and AD began at nearly the same time as the transient and AD-induced increase in [GLU]e. Similarly, the responses to 5% O-2 showed significant delays in the transient depolarization and AD-induced increase in [GLU]e. CBF during 3 or 5% O-2 hypoxic insult was consistently maintained above the control level, i.e., prior to cardiac arrest. Our new dialysis electrode method employing both GOX and ferrocene-conjugated bovine serum albumin allowed evaluation of transient [GLU]e dynamics in the early phase of severe hypoxia in vivo. (C) 1999 Elsevier Science B.V. All rights reserved.