研究人员在小鼠身上找到了一个酶，当该酶在脑中被激活的时候，它看来会增加和维持神经损伤后对疼痛的敏感性。 在受伤的几天之后阻断该酶的作用可减轻疼痛，提示该酶可成为治疗慢性疼痛的一个有前途的标靶。 Xiang-Yao Li及其同事开展了数项聚焦于神经细胞中蛋白激酶M zeta 的分析，这些神经细胞位于脑中的前扣带皮层部分。 神经损伤激活了这些神经元中的该种酶，而这又转而触发了与学习、记忆―以及持续性的对疼痛的感觉。 文章的作者说，这个酶看来与维持慢性疼痛相关的神经元变化有关。
推荐原文出处：
Science DOI: 10.1126/science.1191792
Alleviating Neuropathic Pain Hypersensitivity by Inhibiting PKMζ in the Anterior Cingulate Cortex
Xiang-Yao Li1,2,*, Hyoung-Gon Ko3,*, Tao Chen1,2,*, Giannina Descalzi1, Kohei Koga1, Hansen Wang1, Susan S. Kim1, Yuze Shang1, Chuljung Kwak3, Soo-Won Park3, Jaehoon Shim2,3, Kyungmin Lee3,4, Graham L. Collingridge2,5, Bong-Kiun Kaang2,3,? and Min Zhuo1,2,?
Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, whereas few have addressed the maintenance of plastic changes related to chronic pain. We found that protein kinase M zeta (PKMζ) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC). Peripheral nerve injury caused activation of PKMζ in the ACC, and inhibiting PKMζ by a selective inhibitor, ζ-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation. Microinjection of ZIP into the ACC blocked behavioral sensitization. These results suggest that PKMζ in the ACC acts to maintain neuropathic pain. PKMζ could thus be a new therapeutic target for treating chronic pain.
