Modulation of intracranial meningeal nociceptor activity by cortical spreading depression: a reassessment.

Modulation of intracranial meningeal nociceptor activity by cortical spreading depression: a reassessment.
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皮质扩散抑制对颅内脑膜伤害感受器活性的调节:重新评估。

DOI:
10.1152/jn.00991.2014
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发表时间:
2015
影响因子:
2.5
通讯作者:
Levy,Dan
Levy,Dan
中科院分区:
医学3区
文献类型:
--
作者:
Zhao,Jun;Levy,Dan

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皮质扩散性抑制(CSD),一个假定的偏头痛触发,最近已被证明,以促进多种激活模式的脑膜伤害感受器。在本研究中,我们使用了一种改良的实验方法,在大鼠模型中:1)重新评估单一CSD事件后脑膜伤害感受器的反应,2)检查可能影响CSD后脑膜伤害感受器发展长期激活倾向的因素,3)测试多次CSD后脑膜伤害感受器的反应。一个单一的CSD事件促进持续激活约50%的伤害感受器测试,类似于我们以前的报告。只有两种模式的长期伤害感受器激活观察:双相激活和一个延迟发作。Aδ单位比C单位具有更短的延长激活的平均起始潜伏期。兴奋起始潜伏期的延长与感受野数目呈负相关。CSD后长时间激活的倾向与基础持续活动的存在有关,但既不与CSD阶段短暂激活的出现有关,也不与伤害感受器对炎症介质或ATP的反应有关。最后,与单一CSD相比,多个CSD并没有促进更高的伤害性反应。本研究证实了单一CSD引起脑膜伤害感受器持续激活的能力。CSD诱发的长时间伤害性反应可能与神经元的炎症和ATP化学敏感性无关,而是与其他神经元特性相关,如基础持续活动和感受野数量。
Cortical spreading depression (CSD), a putative migraine trigger, has been shown recently to promote multiple activation patterns of meningeal nociceptors. In the current study we used a modified experimental approach in a rat model to:1) reassess the responses of meningeal nociceptors following a single CSD episode,2) examine factors that may influence the propensity of meningeal nociceptors to develop a prolonged activation following a CSD, and3) test the responses of meningeal nociceptors following multiple CSDs. A single CSD episode promoted persistent activation in about 50% of the nociceptors tested, similar to our previous report. Only two patterns of prolonged nociceptor activation were observed: biphasic activation and one with a delayed onset. Aδ units had shorter mean onset latency for the prolonged activation than C units. The prolonged activation onset latency was inversely correlated with the number of the nociceptors' receptive fields. The propensity to develop the prolonged activation following CSD was related to the presence of basal ongoing activity, but neither to the emergence of brief activation during the CSD phase nor to the nociceptors' responsiveness to inflammatory mediators or ATP. Finally, multiple CSDs did not promote a heightened nociceptive response compared with a single CSD. The present study confirms the ability of a single CSD to elicit persistent activation of meningeal nociceptors. CSD-evoked prolonged nociceptive responses may not be related to the inflammatory and ATP chemosensitivity of the neurons but rather to other neuronal properties, such as basal ongoing activity and number of receptive fields.
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