Site-Specific Regulation of Tau phosphorylation by MAPK pathways during HFS-Induced synaptic plasticity in the Rat hippocampus

IF 2.2 4区医学 Q3 NEUROSCIENCES

Neuroscience Letters Pub Date : 2025-12-10 Epub Date: 2025-10-21 DOI:10.1016/j.neulet.2025.138426

Cem Süer, Burak Tan, Nurcan Dursun, Bilal Koşar, Ercan Babur

引用次数: 0

Abstract

This study examined the role of MAPKs in Tau phosphorylation and synaptic plasticity at perforant pathway–dentate gyrus (PP–DG) synapses following high-frequency stimulation (HFS). In vivo experiments were conducted on adult male Wistar rats under urethane anesthesia. Field potentials (fEPSP and PS) were recorded in the DG granule cell layer in response to PP stimulation. Western blotting assessed total and phosphorylated levels of Tau, ERK1/2, JNK, and P38 MAPK in HFS-induced hippocampus. MAPK inhibition disrupted early somatic potentiation when applied during induction, and JNK inhibition alone impaired late potentiation. Reduced somatic activity correlated with decreased MAPK phosphorylation and Tau phosphorylation at Ser422. Findings suggest that ERK1/2, JNK, and P38 are essential for Tau phosphorylation at Ser422 in HFS-induced hippocampal synapses.

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hfs诱导大鼠海马突触可塑性过程中MAPK通路对Tau磷酸化的位点特异性调控。

本研究探讨了MAPKs在高频刺激（HFS）后穿孔通路-齿状回（PP-DG）突触Tau磷酸化和突触可塑性中的作用。以成年雄性Wistar大鼠为实验对象，在氨基甲酸乙酯麻醉下进行体内实验。在PP刺激下记录DG颗粒细胞层的场电位（fEPSP和PS）。Western blotting检测hfs诱导海马中Tau、ERK1/2、JNK和P38 MAPK的总水平和磷酸化水平。当在诱导过程中应用MAPK抑制时，会破坏早期体细胞增强，而JNK单独抑制会破坏晚期增强。体细胞活性降低与MAPK磷酸化和Tau蛋白Ser422磷酸化降低相关。研究结果表明，ERK1/2、JNK和P38对于hfs诱导的海马突触Ser422位点的Tau磷酸化至关重要。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

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