Aim

To use an animal model of migraine to test whether migraine headache might arise from a brainstem-trigeminal nucleus pathway.

Methods

We measured evoked and spontaneous activity of second-order trigeminovascular neurons in rats to test whether the activity of these neurons increased following the induction of cortical spreading depression or the imposition of light flash – two potential migraine triggers, or headache provokers. We then tested whether drugs that could activate, or inactivate, neurons of the nucleus raphe magnus or the periaqueductal gray matter, would affect any such increases selectively for the dura mater.

Results

Injection of sodium glutamate (a neuronal excitant) into these two nuclei selectively inhibited the responses of trigeminovascular second-order neurons to dura mater, but not to facial skin, stimulation. Injection of lignocaine (a local anaesthetic) into these nuclei selectively potentiated the responses of these neurons to dura, but not to facial skin, stimulation. Furthermore, injections into either nucleus of glutamate inhibited the increase in the ongoing discharge rate of these neurons produced by cortical spreading depression and light flash.

Conclusions

These results provide indirect evidence that trigeminovascular nociception may be tightly controlled by these two nuclei, whereas cutaneous trigeminal sensation may be less so. These nuclei may be relays of one possible brainstem-trigeminal pathway that could mediate migraine headache. Modification of neuronal activity in these two nuclei produced by migraine (headache) triggers may lie behind the pain of a migraine attack, at least in some cases.

中文翻译：

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两个脑干核在颅血管伤害感受和偏头痛触发中的潜在作用

目标

使用偏头痛动物模型来测试偏头痛是否可能由脑干-三叉神经核通路引起。

方法

我们测量了大鼠二阶三叉神经血管神经元的诱发和自发活动，以测试这些神经元的活动是否在诱导皮质扩散抑制或强加闪光后增加 - 两个潜在的偏头痛触发因素或头痛诱发因素。然后我们测试了可以激活或灭活中缝核或导水管周围灰质的神经元的药物是否会选择性地影响硬脑膜的任何此类增加。

结果

将谷氨酸钠（一种神经元兴奋剂）注射到这两个细胞核中可以选择性地抑制三叉神经血管二级神经元对硬脑膜的反应，但对面部皮肤刺激没有反应。将利多卡因（一种局部麻醉剂）注射到这些细胞核中，选择性地增强了这些神经元对硬脑膜的反应，而不是对面部皮肤刺激的反应。此外，向任一谷氨酸核注射可抑制由皮质扩散抑制和闪光产生的这些神经元持续放电率的增加。

结论

这些结果提供了间接证据，表明三叉神经血管伤害感受可能受到这两个核的严格控制，而皮肤三叉神经感觉可能较弱。这些细胞核可能是一种可能介导偏头痛的脑干-三叉神经通路的中继。至少在某些情况下，偏头痛（头痛）触发器产生的这两个核中神经元活动的改变可能是偏头痛发作疼痛的原因。