1 School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.
2 Department of Pharmacology, Wonkwang University School of Medicine, Iksan, Republic of Korea.
Mol Pain. 2018 Jan-Dec;14:1744806918783943. doi: 10.1177/1744806918783943.
Protein kinase M ζ is well known for its role in maintaining memory and pain. Previously, we revealed that the activation of protein kinase M ζ in the anterior cingulate cortex plays a role in sustaining neuropathic pain. However, the mechanism by which protein kinase M ζ is expressed in the anterior cingulate cortex by peripheral nerve injury, and whether blocking of protein kinase M ζ using its inhibitor, zeta inhibitory peptide, produces analgesic effects in neuropathic pain maintained chronically after injury, have not previously been resolved. In this study, we show that protein kinase M ζ expression in the anterior cingulate cortex is enhanced by peripheral nerve injury in a transcription-independent manner. We also reveal that the inhibition of protein kinase M ζ through zeta inhibitory peptide treatment is enough to reduce mechanical allodynia responses in mice with one-month-old nerve injuries. However, the zeta inhibitory peptide treatment was only effective for a limited time.
蛋白激酶 M ζ 因其在维持记忆和疼痛方面的作用而广为人知。先前，我们揭示了前扣带皮层中蛋白激酶 M ζ 的激活在维持神经性疼痛中起作用。然而，外周神经损伤如何导致前扣带皮层中蛋白激酶 M ζ 的表达，以及使用其抑制剂 ζ 抑制肽阻断蛋白激酶 M ζ 是否会在损伤后慢性维持的神经性疼痛中产生镇痛作用，以前尚未解决。在这项研究中，我们表明，外周神经损伤以转录非依赖性方式增强前扣带皮层中的蛋白激酶 M ζ 表达。我们还揭示，通过 ζ 抑制肽处理抑制蛋白激酶 M ζ 足以减少有一个月神经损伤的小鼠的机械性痛觉过敏反应。然而，ζ 抑制肽处理仅在有限的时间内有效。
