University of Arizona, USA.
Cephalalgia. 2011 Jul;31(10):1090-100. doi: 10.1177/0333102411410609. Epub 2011 Jun 23.
Cortical spreading depression (CSD) is a wave of depolarization followed by depression of bioelectrical activity that slowly propagates through the cortex. CSD is believed to be the underlying mechanism of aura in migraine; however, whether CSD can elicit pain associated with migraine headache is unclear.
Awake, freely moving rats were monitored for both CSD events and behavioral responses resulting from dural-cortical pinprick and/or KCl injection to the occipital cortex.
We observed tactile allodynia of the face and hindpaws, as well as enhanced Fos expression within the trigeminal nucleus caudalis (TNC) following CSD induced by KCl injection into the cortex, but not by pinprick. Application of KCl onto the dura elicited cutaneous allodynia and increased Fos staining in the TNC but did not elicit CSD events.
These data suggest that sustained activation of trigeminal afferents that may be required to establish cutaneous allodynia may not occur following CSD events in normal animals.
皮质扩散性抑制(CSD)是一种去极化波,随后是生物电活动的抑制,它缓慢地在皮层中传播。CSD 被认为是偏头痛先兆的潜在机制;然而,CSD 是否会引起与偏头痛头痛相关的疼痛尚不清楚。
在清醒、自由活动的大鼠中,监测到硬脑膜-皮质针刺和/或 KCl 注射到枕叶皮质引起的 CSD 事件以及行为反应。
我们观察到,在 KCl 注射到皮质引起的 CSD 后,面部和后足出现触觉过敏,三叉神经尾核(TNC)中的 Fos 表达增强,但针刺不会引起 CSD 事件。KCl 应用于硬脑膜会引起皮肤过敏和 TNC 中 Fos 染色增加,但不会引起 CSD 事件。
这些数据表明,在正常动物中,CSD 事件后可能不会发生建立皮肤过敏所需的三叉神经传入的持续激活。