Electrophysiological Properties of Dural Afferents in the Absence and Presence of Inflammatory Mediators
Electrophysiological Properties of Dural Afferents in the Absence and Presence of Inflammatory Mediators
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DOI：
10.1152/jn.91339.2008
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发表时间：
2009-06-01
影响因子：
2.5
通讯作者：
Gold, Michael S.
中科院分区：
文献类型：
--
作者：
Harriott, Andrea M.;Gold, Michael S.
有无炎症介质时硬脑膜事件的电生理特性。中国生物医学工程学报（英文版），2009。首次发表于2009年4月1日；doi: 10.1152 / jn.91339.2008。偏头痛是一种使人衰弱的疾病，其特点是反复出现严重的头痛。尽管偏头痛发作的机制仍有争议，但一种说法是炎症介质（IM）诱导的硬脑膜传入事件的激活和敏化有助于偏头痛的开始。我们和其他人已经表明，传入事件的电生理特性，无论是在不存在IM的情况下还是在存在IM的情况下，都随着神经支配目标的功能而变化。这些差异可能解释了与特定身体区域相关的疼痛综合征的独特方面。因此，本研究的目的是验证硬脑膜传入事件的电生理特性不同于支配颞肌（TM）的假设，颞肌是靠近硬脑膜的结构，但与疼痛综合征完全不相关，类似于偏头痛。用全细胞电流钳记录检查支配硬脑膜和TM的急性游离逆行标记初级传入神经。应用IM前后测定被动和主动电生理特性：（mu M）前列腺素E-2(1)，缓激肽（10），组胺(1)。在没有IM的情况下，两个群体之间存在显著差异，特别是在对阈上刺激的反应方面，硬脑膜传入事件比TM传入事件更容易兴奋。重要的是，尽管这两个传入神经群都被IM致敏，但与IM致敏相关的被动和主动电生理变化模式表明，在致敏的潜在机制方面，两者既有相似之处，也有显著差异。如果硬脑膜传入神经和TM传入神经之间的差异是由于离子通道表达的不同模式，而不是相同离子通道的相对密度/生物物理性质的差异，那么可能通过针对im诱导硬脑膜传入神经致敏的不同机制来选择性地治疗偏头痛。
Harriott AM, Gold MS. Electrophysiological properties of dural afferents in the absence and presence of inflammatory mediators. J Neurophysiol 101: 3126-3134, 2009. First published April 1, 2009; doi:10.1152/jn.91339.2008. Migraine is a debilitating condition characterized by recurrent severe head pain. Although mechanisms underlying a migraine attack remain controversial, one proposal is that inflammatory mediator (IM)-induced activation and sensitization of dural afferents contribute to the initiation of migraine pain. We and others have shown that the electrophysiological properties of afferents, both in the absence and the presence of IM, vary as a function of target of innervation. These differences may account for unique aspects of pain syndromes associated with specific body regions. Therefore the purpose of the present study was to test the hypothesis that the electrophysiological properties of dural afferents differ from those innervating the temporalis muscle (TM), a structure in close proximity to the dura but that is not associated with pain syndromes at all similar to migraine. Acutely dissociated retrograde labeled primary afferents innervating the dura and TM were examined with whole cell current-clamp recordings. Passive and active electrophysiological properties were determined before and after the application of IM: (in mu M) prostaglandin E-2 (1), bradykinin (10), and histamine (1). In the absence of IM, there were significant differences between the two populations, particularly with respect to the response to suprathreshold stimulation where dural afferents were more excitable than TM afferents. Importantly, although both populations of afferents were sensitized by IM, the pattern of passive and active electrophysiological changes associated with IM-induced sensitization of these two populations of afferents suggested that there were both similarities and marked differences between the two with respect to underlying mechanisms of sensitization. If the differences between dural and TM afferents are due to a differential pattern of ion channel expression rather than differences in the relative density/biophysical properties of the same ion channels, it may be possible to selectively treat migraine pain by targeting the distinct mechanisms underlying IM-induced sensitization of dural afferents.