Preserved acute pain and reduced neuropathic pain in mice lacking PKC gamma

被引:545
作者
Malmberg, AB
Chen, C
Tonegawa, S
Basbaum, AI
机构
[1] UNIV CALIF SAN FRANCISCO, DEPT PHYSIOL, SAN FRANCISCO, CA 92143 USA
[2] UNIV CALIF SAN FRANCISCO, WM KECK FDN CTR INTEGRAT NEUROSCI, SAN FRANCISCO, CA 92143 USA
[3] MIT, CTR CANC RES, HOWARD HUGHES MED INST, CAMBRIDGE, MA 02139 USA
[4] MIT, DEPT BIOL, CAMBRIDGE, MA 02139 USA
关键词
D O I
10.1126/science.278.5336.279
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:279 / 283
页数:5
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