Thiopental Inhibits Increases in [Ca2+]i Induced by Membrane Depolarization, NMDA Receptor Activation, and Ischemia in Rat Hippocampal and Cortical Slices
Thiopental Inhibits Increases in [Ca2+]i Induced by Membrane Depolarization, NMDA Receptor Activation, and Ischemia in Rat Hippocampal and Cortical Slices
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硫喷妥钠抑制大鼠海马和皮质切片中膜去极化、NMDA 受体激活和缺血引起的 [Ca2]i 增加
作者：
R. Zhan;N. Fujiwara;H. Endoh;T. Yamakura;K. Taga;S. Fukuda;K. Shimoji
本研究检测了硫喷妥钠对由膜去极化、N-甲基-D-天冬氨酸（NMDA）受体激活和缺血引起的细胞内钙（[Ca 2 +]i）变化的影响。方法实验采用Wistar大鼠脑片。[Ca2使用fura-2荧光技术对海马的CA 1锥体细胞层或体感皮层的II至III层进行+]i测量。膜去极化和NMDA受体激活分别通过将切片暴露于60 mM K+和100 [micro sign]M NMDA诱导。通过用95%氮气和5%二氧化碳平衡的无葡萄糖Krebs溶液灌注切片来诱导体外缺血。硫喷妥钠在高K+和NMDA应用前5 min或在离体缺血前应用。结果缺血15 min，海马和皮质脑片[Ca 2 +]i均出现特征性升高。硫喷妥钠可延长缺血后8、10、15 min [Ca ~（2+）]i平台期的潜伏期，降低[Ca ~（2+）]i的升高幅度。硫喷妥钠还抑制高K+-和NMDA-诱导的[Ca（2+）]i增加。皮层脑片中NMDA诱导的[Ca 2 +]i增加的衰减程度大于海马脑片。在培养的皮层神经元中证实了硫喷妥钠对200-[micro sign]M NMDA-介导的[Ca 2 +]i反应的抑制作用。结论硫喷妥钠可抑制海马和皮层缺血引起的[Ca 2 +]i升高，其机制可能与抑制电压门控性钙通道和NMDA受体有关。硫喷妥钠对NMDA受体的区域性抑制可能与其抗缺血的区域特异性作用有关。
Background This study examined the effects of thiopental on intracellular calcium ([Ca2+]i) changes induced by membrane depolarization, N‐methyl‐D‐aspartate (NMDA) receptor activation, and ischemia. Methods Experiments were performed in brain slices prepared from Wistar rats. [Ca2+]i measurements were taken on the CA1 pyramidal cell layer of the hippocampus or layers II to III of the somatosensory cortex using the fura‐2 fluorescence technique. Membrane depolarization and NMDA receptor activation were induced by exposing slices to 60 mM K+ and 100 [micro sign]M NMDA, respectively. In vitro ischemia was induced by superfusing slices with glucose‐free Krebs solution equilibrated with 95% nitrogen and 5% carbon dioxide. Thiopental was applied 5 min before application of high K+ and NMDA, or before in vitro ischemia. Results Ischemia for 15 min produced a characteristic [Ca2+]i increase in both hippocampal and cortical slices. Thiopental prolonged the latency to the appearance of the [Ca2+]i plateau and reduced the magnitudes of increase in [Ca2+]i 8, 10, and 15 min after the onset of ischemia. Thiopental also suppressed the high K+‐and NMDA‐induced [Ca (2+)]i increases. The NMDA‐induced [Ca2+]i increases were attenuated to a greater extent in cortical slices than were those in hippocampal slices. The inhibition of thiopental on the 200‐[micro sign]M NMDA‐mediated [Ca2+]i response was confirmed in cultured cortical neurons. Conclusions The results indicate that thiopental attenuates ischemia‐induced [Ca2+]i increases in the hippocampus and cortex in vitro, probably because of its inhibition of both voltage‐gated calcium channels and NMDA receptors. The regionally different inhibition of thiopental on NMDA receptors may relate to its region‐specific action against ischemia.
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影响因子：
4
作者：
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通讯作者：
Brockerhoff,H
DOI：
10.1016/0925-4439(95)00015-v
发表时间：
1995-05-24
影响因子：
6.2
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DOI：
10.1113/jphysiol.1993.sp019805
发表时间：
1993
期刊：
The Journal of physiology
影响因子：
--
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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