Chronic degeneration of dorsal raphe serotonergic neurons modulates cortical spreading depression: A possible pathophysiology of migraine
Chronic degeneration of dorsal raphe serotonergic neurons modulates cortical spreading depression: A possible pathophysiology of migraine
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DOI：
10.1002/jnr.23209
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发表时间：
2013-06
影响因子：
4.2
通讯作者：
Yilong Cui;Qing-hua Li;H. Yamada;Yasuyoshi Watanabe;Y. Kataoka
中科院分区：
文献类型：
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作者：
Yilong Cui;Qing-hua Li;H. Yamada;Yasuyoshi Watanabe;Y. Kataoka
偏头痛的病理生理学与脑内的血管肾上腺素能系统有关，然而，脑实质的肾上腺素能神经系统在病理生理学中的参与仍不清楚。为了研究脑实质多巴胺能神经系统是否参与偏头痛的病因学，我们通过产生皮质扩散性抑制（SD）制备了偏头痛的实验模型，其特征在于神经元/胶质细胞膜去极化的扩散伴随着整个大鼠大脑皮质半球的脑血流量（CBF）的暂时升高，其接受了中缝背核中5-羟色胺能神经元变性的药物治疗。我们发现：1）治疗组大鼠中缝背核中的多巴胺能神经元和大脑皮层中的多巴胺能纤维明显变性，2）这些大鼠CBF变化的扩散速度明显增加，3）这些大鼠计算的去极化波宽度明显延长。这些结果表明，中缝背核多巴胺能神经元调节皮层扩散性抑制，并可能通过类似的机制参与偏头痛的病理过程。© 2013 Wiley Periodicals，Inc.
The vascular serotonergic system in the brain has been implicated in the pathophysiology of migraine, however, involvement of the serotonergic nervous system of the brain parenchyma in the pathophysiology remains unclear. To investigate whether the brain parenchymal serotonergic nervous system is involved in the etiology of migraine, we prepared an experimental model of migraine by generation of cortical spreading depression (SD), characterized by spreading of neuronal/glial membrane depolarization accompanied by temporal elevation of the cerebral blood flow (CBF) throughout the cerebral cortical hemisphere in rats, which underwent pharmacological treatment for degeneration of serotonergic neurons in the dorsal raphe nucleus. We show here that 1) significant degeneration of serotonergic neurons in the dorsal raphe nucleus and serotonergic fibers in the cerebral cortex was observed in treated rats, 2) spreading velocity of the CBF changes was significantly increased in these rats, and 3) calculated width of the depolarization wave was significantly extended in these rats. These results indicate that the dorsal raphe serotonergic neurons modulate cortical spreading depression and might be involved in migraine pathology via a similar mechanism. © 2013 Wiley Periodicals, Inc.