Department of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, 2177 Dalgubeol-daero, Daegu, 41940, South Korea.
Department of Biological Sciences, College of Natural Sciences, Seoul National University, 1 Gwanangno, Gwanak-gu, Seoul, 08826, South Korea.
Mol Brain. 2020 Feb 12;13(1):19. doi: 10.1186/s13041-020-0564-y.
Synaptic proteins play an important role for the regulation of synaptic plasticity. Numerous studies have identified and revealed individual synaptic protein functions using protein overexpression or deletion. In neuropathic pain nociceptive stimuli conveyed from the periphery repetitively stimulate neurons in the central nerve system, brain and spinal cord. Neuronal activities change the turnover (synthesis and degradation) rate of synaptic proteins. Thus, the analysis of synaptic protein turnover rather than just expression level change is critical for studying the role of synaptic proteins in synaptic plasticity. Here, we analyzed synaptosomal proteome in the anterior cingulate cortex (ACC) to identify protein turnover rate changes caused by peripheral nerve injury. Whereas PKCγ levels were not altered, we found that the protein's turnover rate decreased after peripheral nerve injury. Our results suggest that postsynaptic PKCγ synthesized by neuronal activities in the ACC is translocated to the postsynaptic membrane with an extended half-life.
突触蛋白在调节突触可塑性方面发挥着重要作用。许多研究已经通过蛋白质过表达或缺失来鉴定和揭示单个突触蛋白的功能。在神经病理性疼痛中,来自外周的伤害性刺激会反复刺激中枢神经系统、大脑和脊髓中的神经元。神经元活动改变突触蛋白的周转率(合成和降解)。因此,分析突触蛋白的周转率而不仅仅是表达水平的变化对于研究突触蛋白在突触可塑性中的作用至关重要。在这里,我们分析了前扣带皮层 (ACC) 的突触体蛋白质组,以确定外周神经损伤引起的蛋白质周转率变化。虽然 PKCγ 的水平没有改变,但我们发现外周神经损伤后其周转率下降。我们的结果表明,ACC 神经元活动合成的突触后 PKCγ 通过延长半衰期被转运到突触后膜。