Cortical spreading depolarisation (CSD), the neural mechanism underlying migraine aura, may cause headache by sensitising the trigeminal system. Photophobia, the most bothersome accompanying symptom during migraine attacks, is more prevalent in migraine with aura than in migraine without aura. Whether CSD plays a role in developing photophobia remains unknown. Moreover, migraine-induced physical hypoactivity contributes to loss of productivity. We aimed to investigate the development of trigeminal sensitisation, photophobia and locomotive abnormality after KCl-induced CSD using 86 male C57BL/6 mice. Sham-operated mice were used as controls. We confirmed the presence of trigeminal sensitisation and photophobia at 24 h after CSD. CSD-subjected mice also exhibited significantly reduced locomotive activity in both light and dark zones. Hence, the CSD-induced hypomobility was likely to be independent of photophobia. The 5-HT_1B/1D agonist, sumatriptan, corrected all these CSD-induced abnormalities. Moreover, dose dependency was demonstrated in the ameliorating effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, olcegepant, on these abnormalities. Sumatriptan and olcegepant improved mouse locomotion with therapeutic lags ranging from 20 to 30 min. Collectively, CSD caused trigeminal sensitisation, photophobia and hypomobility that persisted for at least 24 h by a mechanism involving the 5-HT_1B/1D and CGRP activity.

皮质扩散去极化 (CSD) 是偏头痛先兆的神经机制，可能通过使三叉神经系统敏感而引起头痛。畏光是偏头痛发作时最令人烦恼的伴随症状，有先兆偏头痛比无先兆偏头痛更常见。 CSD 是否在畏光的发生过程中发挥作用仍不清楚。此外，偏头痛引起的身体活动不足会导致生产力下降。我们的目的是使用 86 只雄性 C57BL/6 小鼠研究 KCl 诱导 CSD 后三叉神经敏感、畏光和运动异常的发展情况。使用假手术小鼠作为对照。我们证实 CSD 后 24 小时存在三叉神经过敏和畏光。接受 CSD 治疗的小鼠在明区和暗区的运动活动也显着降低。因此，CSD 引起的活动能力低下可能与畏光无关。 5-HT _1B/1D激动剂舒马曲坦纠正了所有这些 CSD 引起的异常。此外，降钙素基因相关肽 (CGRP) 受体拮抗剂 olcegepant 对这些异常的改善作用显示出剂量依赖性。舒马普坦和奥塞格泮改善了小鼠的运动能力，治疗滞后范围为 20 至 30 分钟。总的来说，CSD 通过涉及 5-HT _1B/1D和 CGRP 活性的机制引起三叉神经敏感、畏光和活动能力下降，并持续至少 24 小时。