研究人員在小鼠身上找到了一個(gè)酶,，當(dāng)該酶在腦中被激活的時(shí)候,，它看來(lái)會(huì)增加和維持神經(jīng)損傷后對(duì)疼痛的敏感性,。 在受傷的幾天之后阻斷該酶的作用可減輕疼痛，提示該酶可成為治療慢性疼痛的一個(gè)有前途的標(biāo)靶,。 Xiang-Yao Li及其同事開(kāi)展了數(shù)項(xiàng)聚焦于神經(jīng)細(xì)胞中蛋白激酶M zeta 的分析,，這些神經(jīng)細(xì)胞位于腦中的前扣帶皮層部分,。 神經(jīng)損傷激活了這些神經(jīng)元中的該種酶，而這又轉(zhuǎn)而觸發(fā)了與學(xué)習(xí),、記憶—以及持續(xù)性的對(duì)疼痛的感覺(jué),。 文章的作者說(shuō)，這個(gè)酶看來(lái)與維持慢性疼痛相關(guān)的神經(jīng)元變化有關(guān),。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
