Prince of Wales Clinical School, UNSW (Sydney), NSW, Australia.
Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW, Australia.
Cephalalgia. 2021 Feb;41(2):203-216. doi: 10.1177/0333102420960039. Epub 2020 Sep 29.
To use an animal model of migraine to test whether migraine headache might arise from a brainstem-trigeminal nucleus pathway.
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.
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.
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.
利用偏头痛动物模型来检验偏头痛头痛是否可能源于脑干-三叉神经核通路。
我们测量了大鼠二级三叉血管神经元的诱发和自发性活动，以检验皮质扩散性抑制或光闪（两种潜在的偏头痛触发因素或头痛诱发因素）诱导后这些神经元的活动是否增加。然后，我们测试了能够激活或失活中缝大核或导水管周围灰质神经元的药物是否会选择性地影响这些神经元对硬脑膜的任何这种增加。
将谷氨酸钠（神经元兴奋剂）注射到这两个核中，选择性地抑制了三叉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（局部麻醉剂）注射到这些核中，选择性地增强了这些神经元对硬脑膜的反应，但对面部皮肤刺激没有反应。此外，将谷氨酸注入任一核中，可抑制皮质扩散性抑制和光闪引起的这些神经元持续放电率的增加。
这些结果提供了间接证据，表明三叉血管伤害感受可能受到这两个核的紧密控制，而皮肤三叉神经感觉则可能不太受控制。这些核可能是介导偏头痛头痛的可能的脑干-三叉神经通路的中继站。偏头痛（头痛）触发因素引起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背后原因，至少在某些情况下是这样。
