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首页> 外文期刊>Journal of Cellular Physiology >The Cholinergic Signaling Responsible for the Expression of a Memory-Related Protein in Primary Rat Cortical Neurons
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The Cholinergic Signaling Responsible for the Expression of a Memory-Related Protein in Primary Rat Cortical Neurons

机译：胆碱能信号负责在主要与内存相关蛋白的表达大鼠皮层神经元

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摘要

Cholinergic dysfunction in the brain is closely related to cognitive impairment including memory loss. In addition to the degeneration of basal forebrain cholinergic neurons, deficits in the cholinergic receptor signaling may also play an important role. In the present study, to examine the cholinergic signaling pathways responsible for the induction of a memory-related postsynaptic protein, a cholinergic agonist carbachol was used to induce the expression of activity-regulated cytoskeleton associated protein (Arc) in primary rat cortical neurons. After pretreating neurons with various antagonists or inhibitors, the levels of carbachol-induced Arc protein expression were detected by Western blot analysis. The results show that carbachol induces Arc protein expression mainly through activating M1 acetylcholine receptors and the downstream phospholipase C pathway, which may lead to the activation of the MAPK/ERK signaling pathway. Importantly, carbachol-mediated M2 receptor activation exerts negative effects on Arc protein expression and thus counteracts the enhanced effects of M1 activation. Furthermore, it is suggested for the first time that M1-mediated enhancement of N-methyl-D-aspartate receptor (NMDAR) responses, leading to Ca2+ entry through NMDARs, contributes to carbachol-induced Arc protein expression. These findings reveal a more complete cholinergic signaling that is responsible for carbachol-induced Arc protein expression, and thus provide more information for developing treatments that can modulate cholinergic signaling and consequently alleviate cognitive impairment. (C) 2016 Wiley Periodicals, Inc.
机译：胆碱能功能障碍在大脑密切与认知障碍包括内存有关的损失。前脑胆碱能神经元,赤字的胆碱能受体信号也可能发挥重要的作用。胆碱能信号通路负责与内存相关的感应突触后蛋白质,胆碱能受体激动剂氯化氨甲酰胆碱诱导的表达activity-regulated细胞骨架相关蛋白质(电弧)主要鼠皮质神经元。粗加工后神经元与不同拮抗剂和抑制剂的水平carbachol-induced弧蛋白表达检测到免疫印迹分析。表明碳酰胆碱诱发弧蛋白质表达主要是通过激活M1乙酰胆碱受体和下游磷脂酶C通路,这可能会导致MAPK / ERK信号通路的激活。重要的是,carbachol-mediated M2受体对弧蛋白质激活产生负面影响表达式,从而抵消增强M1激活的影响。建议第一次M1-mediated增强的n -甲基- d受体(NMDAR)反应,导致Ca2 +条目NMDARs,有助于carbachol-induced弧蛋白表达。胆碱能完成信号负责carbachol-induced弧蛋白质表达式,从而提供更多的信息开发治疗,可以调节胆碱能信号,从而缓解认知障碍。公司。

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