PKMζ Is Not Required for Development of Postsurgical Pain.

PKMζ Is Not Required for Development of Postsurgical Pain.
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术后疼痛的发生不需要 PKM zeta

DOI:
10.1007/s12035-017-0499-1
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发表时间:
2018-03
影响因子:
5.1
通讯作者:
Tao F
Tao F
中科院分区:
医学2区
文献类型:
--
作者:
Liu S;Li C;Guo Y;Xing Y;Tao F

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先前的研究表明,蛋白激酶M Zeta(PKMζ)是一种脑特有的蛋白激酶C亚型,通过合成Zeta抑制肽参与几种疼痛模型中伤害性感觉的中枢处理。在本研究中,我们利用条件性和传统性PKMζ基因敲除小鼠,研究了PKMζ是否参与了术后疼痛的发病机制。结果表明,注射他莫昔芬后,条件性PKMζ基因敲除小鼠的前扣带回皮质中PKMζ的表达受到抑制,但脊髓未见表达。条件性pKMζ基因敲除小鼠与野生型小鼠在足底切开后产生的疼痛反应相似。此外,常规PKMζ基因敲除小鼠的前扣带回皮质和脊髓中PKMζ的表达均受到抑制。野生型、杂合型和纯合型常规pKMζ基因敲除小鼠术后疼痛发生率无显著差异。这些数据表明,ζ对于足底切开术后疼痛的发生不是必需的。
Previous studies have shown that protein kinase M zeta (PKMζ), a brain-specific isoform of protein kinase C, is involved in the central processing of nociception in several pain models by using a synthetic zeta inhibitory peptide. In the present study, we investigated whether PKMζ contributes to the pathogenesis of postsurgical pain using both conditional and conventional PKMζ knockout mice. Our results showed that the expression of PKMζ in anterior cingulate cortex, but not spinal cord, of the conditional PKMζ knockout mice was inhibited following tamoxifen injection. And the conditional PKMζ knockout mice displayed similar plantar incision-produced postsurgical pain responses as those in wild-type mice. Moreover, the expression of PKMζ was inhibited in both anterior cingulate cortex and spinal cord of the conventional PKMζ knockout mice. And there were no significant differences in the development of postsurgical pain among wild-type, heterozygous and homozygous conventional PKMζ knockout mice. These data suggest that PKMζ is not required for the development of postsurgical pain after plantar incision.
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