Activation of central trigeminovascular neurons by cortical spreading depression.
Activation of central trigeminovascular neurons by cortical spreading depression.
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DOI：
10.1002/ana.22329
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发表时间：
2011-05
影响因子：
11.2
通讯作者：
Burstein, Rami
中科院分区：
文献类型：
--
作者：
Zhang, XiChun;Levy, Dan;Kainz, Vanessa;Noseda, Rodrigo;Jakubowski, Moshe;Burstein, Rami
皮质扩散性抑制（CSD）长期以来被认为与开始有视觉先兆的偏头痛发作有关。已经证明CSD波可以触发脑膜伤害感受器的持久激活-三叉神经血管通路的一级神经元被认为是偏头痛的基础-我们现在报告CSD可以激活三叉神经脊束核（C1 - 2）中的中央三叉神经血管神经元。用针刺或KCl颗粒刺激皮层诱发CSD。在麻醉大鼠中使用单单位记录监测C1 - 2中的神经元活性。在CSD激活的25个三叉神经血管神经元中，（峰值/秒）从CSD前的3.6 ± 1.2增加（基线）至CSD后6.1 ± 1.8（p <0.0001），14个单位的神经元活性在30.0 ± 3.1分钟后恢复到基线水平，其余11个单位在整个记录期间持续升高66.0 ± 8.3（22 - 108）min。神经元激活开始于0.9 ± 0.4 27个未被CSD激活的三叉神经血管神经元中，9个位于I~II层，9个位于III~V层，潜伏期为25.1 ± 4.0（7-75）min。基线时平均放电频率为2.0 ± 0.7，CSD后为1.8 ± 0.7。我们建议，CSD构成一种伤害性刺激，能够激活周围和中央三叉神经血管神经元的基础偏头痛的先兆。
Cortical spreading depression (CSD) has long been implicated in migraine attacks that begin with visual aura. Having shown that a wave of CSD can trigger long-lasting activation of meningeal nociceptors – the first-order neurons of the trigeminovascular pathway thought to underlie migraine headache – we now report that CSD can activate central trigeminovascular neurons in the spinal trigeminal nucleus (C1-2). Stimulation of the cortex with pin prick or KCl granule was used to induce CSD. Neuronal activity was monitored in C1-2 using single-unit recording in anesthetized rats. In 25 trigeminovascular neurons activated by CSD, mean firing rate (spikes/sec) increased from 3.6 ± 1.2 before CSD (baseline) to 6.1 ± 1.8 after CSD (p < 0.0001) for a period >13 min. Neuronal activity returned to baseline level after 30.0 ± 3.1 min in 14 units, and remained elevated for 66.0 ± 8.3 (22–108) min through the entire recording period in the other 11 units. Neuronal activation began within 0.9 ± 0.4 (0–2.5) min after CSD in 7 neurons located in laminae I-II, or after a latency of 25.1 ± 4.0 (7–75) min in 9 neurons located in laminae I-II, and 9 neurons located in laminae III-V. In 27 trigeminovascular neurons not activated by CSD, mean firing rate was 2.0 ± 0.7 at baseline and 1.8 ± 0.7 after CSD. We propose that CSD constitutes a nociceptive stimulus capable of activating peripheral and central trigeminovascular neurons that underlie the headache of migraine with aura.
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影响因子：
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