Preserved acute pain and reduced neuropathic pain in mice lacking PKC gamma
Preserved acute pain and reduced neuropathic pain in mice lacking PKC gamma
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DOI：
10.1126/science.278.5336.279
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发表时间：
1997-10-10
期刊：
影响因子：
56.9
通讯作者：
Basbaum, AI
中科院分区：
文献类型：
--
作者：
Malmberg, AB;Chen, C;Basbaum, AI
在正常动物中，周围神经损伤产生一种持续的神经性疼痛状态，这种疼痛被夸大，可以由非疼痛性刺激产生。在这里，缺乏蛋白激酶C γ (PKC γ)的小鼠对急性疼痛刺激表现出正常的反应，但在部分坐骨神经切除后，它们几乎完全没有发生神经性疼痛综合征，神经损伤后脊髓发生的神经化学变化被钝化。此外，PKC γ被证明局限于背角神经元的一小部分，从而确定了预防和治疗持续性疼痛的潜在生化靶点。
In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack protein kinase C gamma (PKC gamma) displayed normal responses to acute pain stimuli, but they almost completely failed to develop a neuropathic pain syndrome after partial sciatic nerve section, and the neurochemical changes that occurred in the spinal cord after nerve injury were blunted. Also, PKC gamma was shown to be restricted to a small subset of dorsal horn neurons, thus identifying a potential biochemical target for the prevention and therapy of persistent pain.