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首页> 外文期刊>American Journal of Physiology >Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during N-methyl-D-aspartate superfusion.
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Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during N-methyl-D-aspartate superfusion.

机译：N-甲基-D-天门冬氨酸超融合过程中，皮质扩散性抑郁症混淆了浓度依赖性的小动脉扩张。

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摘要

Pial arterioles do not express N-methyl-D-aspartate (NMDA) receptors but dilate in response to topical NMDA application. We explored the mechanism underlying NMDA-mediated responses in murine pial arterioles (11-31 microm), using a closed cranial window preparation, and found that arteriolar dilation was not concentration dependent. Pial arteriolar diameter abruptly increased within 3 min of superfusing 50 or 100 microM NMDA. Dilation reached a peak within 1 min (46 +/- 14%) and then declined to a plateau (28 +/- 13%) for the duration of superfusion. Whereas a higher concentration (200 microM) did not produce further dilation, lower concentrations (1-10 microM) did not dilate the arterioles at all. MK-801 (10 microM) abrogated the dilation response, whereas Nomega-nitro-L-arginine (1 mM) attenuated the peak and abolished the sustained dilation during NMDA superfusion. We determined that NMDA-induced pial arteriolar responses were evoked by cortical spreading depression, because abrupt vasodilation during 50 or 100 microM NMDA superfusion was associated with a large negative slow potential shift and electrocorticogram suppression that spread from the superfusion window to distant cortical areas. Our data suggest that the responses of pial arterioles to NMDA are caused in part by neurovascular coupling due to cortical spreading depression.
机译：颈小动脉不表达N-甲基-D-天冬氨酸（NMDA）受体，但会因局部NMDA的应用而扩张。我们探索了NMDA介导的小鼠皮层小动脉（11-31微米）的潜在反应的机制，使用封闭的颅窗准备，并发现小动脉扩张不依赖于浓度。在融合50或100 microM NMDA的3分钟内，小叶小动脉直径突然增加。扩张在1分钟内达到峰值（46 +/- 14％），然后在灌注持续时间内下降至平稳期（28 +/- 13％）。较高的浓度（200 microM）不会产生进一步的扩张，而较低的浓度（1-10 microM）则根本不会扩张小动脉。 MK-801（10 microM）消除了扩张反应，而Nomega-nitro-L-精氨酸（1 mM）减弱了峰并取消了NMDA融合过程中的持续扩张。我们确定NMDA诱导的皮层小动脉反应是由皮质扩散抑制引起的，因为在50或100 microM NMDA融合过程中突然的血管舒张与大的负缓慢电位偏移和皮质电图抑制相关，后者从融合窗口扩散到远处的皮质区域。我们的数据表明，对皮层小动脉对NMDA的反应部分是由于皮层扩散抑制所致的神经血管耦合引起的。

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