PKCγ contributes to a subset of the NMDA-dependent spinal circuits that underlie injury-induced persistent pain
PKCγ contributes to a subset of the NMDA-dependent spinal circuits that underlie injury-induced persistent pain
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DOI：
10.1523/jneurosci.21-14-05321.2001
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发表时间：
2001-07-15
影响因子：
5.3
通讯作者：
Basbaum, AI
中科院分区：
文献类型：
--
作者：
Martin, WJ;Malmberg, AB;Basbaum, AI
在以前的研究中，我们提供的证据表明，蛋白激酶C（PKC γ）的γ亚型是一个重要的贡献者增加疼痛的敏感性，发生在受伤后。在此，我们在野生型和PKC γ-缺失小鼠中结合电生理学和行为方法，以比较脊髓背角第V层中宽动态范围神经元的超兴奋性与由相同损伤产生的行为超兴奋性[将C-纤维刺激物芥子油（MO）应用于后爪]。野生型和无效小鼠在组织损伤前对机械或热刺激的反应没有差异，并且对MO刺激的反应幅度相当。在野生型小鼠中，MO使V层神经元对无害的机械和热刺激的反应显著和进行性增强。神经元过度兴奋的时间过程与MO诱导的行为异常性疼痛（响应于先前无害的机械刺激的伤害性行为）的时间过程一致。PKC γ基因敲除小鼠也表现出神经元的过度兴奋，但这种过度兴奋持续时间较长。
In previous studies we provided evidence that the gamma isoform of protein kinase C (PKC gamma) is an important contributor to the increased pain sensitivity that occurs after injury. Here we combined electrophysiological and behavioral approaches in wild-type and PKC gamma -null mice to compare the hyperexcitability of wide dynamic range neurons in lamina V of the spinal cord dorsal horn with the behavioral hyperexcitability produced by the same injury [application of a C-fiber irritant, mustard oil (MO), to the hindpaw]. Wild-type and null mice did not differ in their response to mechanical or thermal stimuli before tissue injury, and the magnitude of the response to the MO stimuli was comparable. in wild-type mice, MO produced a dramatic and progressive enhancement of the response of lamina V neurons to innocuous mechanical and thermal stimuli. The time course of the neuronal hyperexcitability paralleled the time course of the MO-induced behavioral allodynia (nocifensive behavior in response to a previously innocuous mechanical stimulus). Neuronal hyperexcitability was also manifest in the PKC gamma -null mice, but it lasted