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首页> 外文期刊>Brain research >Increased tyrosine phosphorylation of alpha(1C) subunits of L-type voltage-gated calcium channels and interactions among Src/Fyn, PSD-95 and alpha(1C) in rat hippocampus after transient brain ischemia.
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Increased tyrosine phosphorylation of alpha(1C) subunits of L-type voltage-gated calcium channels and interactions among Src/Fyn, PSD-95 and alpha(1C) in rat hippocampus after transient brain ischemia.

机译：L型电压门控钙通道的alpha（1C）亚基的酪氨酸磷酸化增加以及短暂性脑缺血后大鼠海马中Src / Fyn，PSD-95和alpha（1C）之间的相互作用。

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It has been reported that the Src family kinases-mediated tyrosine phosphorylation of alpha(1C) subunits of L-type voltage-gated calcium channels (L-VGCCs) potentiates the channel currents. In this study, we evaluated the alterations in the tyrosine phosphorylation level of alpha(1C) and in the interactions involving Src/Fyn, alpha(1C) and PSD-95 in the hippocampus after transient (15 min) brain ischemia followed by various times of reperfusion using immunoprecipitation and immunoblotting. Transient brain ischemia was induced by the method of four-vessel occlusion in Sprague-Dawley rats. The tyrosine phosphorylation level of alpha(1C) subunits elevated immediately after brain ischemia. The elevation in phosphorylation sustained for at least 6 h and peaked at 15 min of reperfusion. Transient brain ischemia and reperfusion also caused rapid and sustained increases in the interactions of Src and Fyn with alpha(1C) subunits. More interestingly, co-immunoprecipitation analysis showed that 15 min of reperfusion dramatically increased the interaction between PSD-95 and alpha(1C) and promoted the formation of alpha(1C)-PSD-95-Src complexes, for the first time. The protein levels of alpha(1C), Src, Fyn and PSD-95 showed no differences at all time points. These results suggest a novel mechanism involving the ischemia/reperfusion-induced recruitment of L-VGCCs, Src and Fyn to the PSD-95 signaling complex that facilitates the tyrosine phosphorylation of alpha(1C) subunits by Src family kinases and may contribute to the up-regulation of L-VGCCs activity in postischemic hippocampus.
机译：据报道，Src家族激酶介导的L型电压门控钙通道（L-VGCC）的alpha（1C）亚基的酪氨酸磷酸化增强了通道电流。在这项研究中，我们评估了短暂（15分钟）脑缺血后不同时间海马体中α（1C）酪氨酸磷酸化水平以及涉及Src / Fyn，α（1C）和PSD-95的相互作用的变化免疫沉淀和免疫印迹检测再灌注通过四血管闭塞法在Sprague-Dawley大鼠中诱发短暂性脑缺血。脑缺血后，α（1C）亚基的酪氨酸磷酸化水平立即升高。磷酸化的升高持续至少6小时，并在再灌注15分钟时达到峰值。短暂性脑缺血和再灌注也引起Src和Fyn与alpha（1C）亚基相互作用的快速和持续增加。更有趣的是，免疫共沉淀分析显示15分钟的再灌注显着增加了PSD-95与alpha（1C）之间的相互作用，并首次促进了alpha（1C）-PSD-95-Src复合物的形成。 α（1C），Src，Fyn和PSD-95的蛋白质​​水平在所有时间点均无差异。这些结果表明涉及缺血/再灌注诱导的L-VGCC，Src和Fyn募集到PSD-95信号复合物的新机制，该机制促进Src家族激酶对alpha（1C）亚基的酪氨酸磷酸化，并可能有助于缺血后海马中L-VGCCs活性的调节

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