Borysovych Bogdanov Volodymyr, Bogdanova Olena Viktorivna, Lombard Arnaud, Chauvel Virginie, Multon Sylvie, Kot Larysa Ivanivna, Makarchuk Mykola Yukhymovych, Schoenen Jean
Giga-Neurosciences, Headache Research Unit, University of Liege, Liege 4000, Belgium; Taras Shevchenko National University of Kyiv, Volodymyrska Str. 64, Kyiv 01033, Ukraine; INRA, Nutrition et Neurobiologie Intégrée and University Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, 146 Rue Léo-Saignat, Bordeaux Cedex 33076, France.
Taras Shevchenko National University of Kyiv, Volodymyrska Str. 64, Kyiv 01033, Ukraine.
Neurosci Lett. 2015 Jan 12;585:138-43. doi: 10.1016/j.neulet.2014.11.026. Epub 2014 Nov 20.
The migraine headache involves activation and central sensitization of the trigeminovascular pain pathway. The migraine aura is likely due to cortical spreading depression (CSD), a propagating wave of brief neuronal depolarization followed by prolonged inhibition. The precise link between CSD and headache remains controversial. Our objectives were to study the effect of CSD on neuronal activation in the periaqueductal grey matter (PAG), an area known to control pain and autonomic functions, and to be involved in migraine pathogenesis. Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia. Being part of a pharmacological study, six animals had received, for the preceding 4 weeks daily, intraperitoneal injections of lamotrigine (15 mg/kg), six others had been treated with saline, while five sham-operated animals served as controls. We found that the number of Fos-immunoreactive nuclei in the PAG decreased after CSD provocation. There was no difference between lamotrigine- and saline-treated animals. The number of CSDs correlated negatively with Fos-immunoreactive counts. CSD-linked inhibition of neuronal activity in the PAG might play a role in central sensitization during migraine attacks and contribute to a better understanding of the link between the aura and the headache.
偏头痛涉及三叉神经血管疼痛通路的激活和中枢敏化。偏头痛先兆可能是由于皮质扩散性抑制（CSD），即一种短暂神经元去极化后接着长时间抑制的传播性波。CSD与头痛之间的确切联系仍存在争议。我们的目的是研究CSD对导水管周围灰质（PAG）神经元激活的影响，PAG是一个已知控制疼痛和自主功能且参与偏头痛发病机制的区域。在水合氯醛麻醉下，对17只成年雄性Sprague-Dawley大鼠进行氯化钾诱导的CSD后，计数其延髓头端PAG和动眼神经副核（PAG-EWn，前囟-6.5毫米）以及延髓尾端PAG（前囟-8毫米）中Fos免疫反应性细胞核的数量。作为一项药理学研究的一部分，6只动物在之前4周每天接受腹腔注射拉莫三嗪（15毫克/千克），另外6只接受生理盐水治疗，同时5只假手术动物作为对照。我们发现，CSD激发后PAG中Fos免疫反应性细胞核的数量减少。拉莫三嗪治疗组和生理盐水治疗组动物之间没有差异。CSD的次数与Fos免疫反应性计数呈负相关。CSD相关的PAG神经元活动抑制可能在偏头痛发作期间的中枢敏化中起作用，并有助于更好地理解先兆与头痛之间的联系。
