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降低CaMKII的基化导致老化相关的记忆和突触可塑性损伤在小鼠中

Nicole L Rumian^1,2, Ronald K Freund¹, Mark L Dell'Acqua^1,2

¹Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Science signaling

|July 25, 2023

概括

-芽素-依赖蛋白激酶II (CaMKII) 化对记忆和突触可塑性至关重要. 在CaMKII中化受损导致记忆缺陷和减少长期潜能,模仿衰老效应.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
生物化学生化学

背景情况:

-芽素依赖蛋白激酶II (CaMKII) 通过自酸化和GluN2B结合表现出分子记忆.
化和氧化是影响CaMKII自主性和功能的其他机制.
衰老与CaMKII化减少和突触可塑性受损有关.

研究的目的:

研究CaMKII化和氧化在神经元功能,记忆和突触可塑性中的作用.
描述受损的CaMKII化/氧化对记忆和长期潜能 (LTP) 的影响.
为了比较CaMKII突变小鼠中的功能缺陷与老野生型小鼠中观察到的功能缺陷.

主要方法:

产生了一种模拟小鼠系 (CaMKII^ΔSNO) 的突变,使 CaMKII调控域的化/氧化无能.
评估记忆和突触可塑性,使用行为测试和电生理学记录 (通过甲爆刺激和高频刺激诱导LTP).
研究了L型电压通道在CaMKII^ΔSNO小鼠和老野生型小鼠中HFS-LTP中的作用.
在海马神经元中研究了CaMKII突触局部化和化状态.

主要成果:

CaMKII^ΔSNO小鼠表现出记忆和突触可塑性的缺陷,反映了老年野生型小鼠.
在CaMKII^ΔSNO小鼠中,theta爆刺激诱导的LTP降低,类似于在老年小鼠中使用低化CaMKII的老鼠.
年轻成年CaMKII小鼠和老年野生型小鼠的HFS-LTP需要L型电压通道.
与衰老相关的损伤与减少的CaMKII化有关,而不是氧化.
化诱导的基底突触CaMKII积累通过GluN2B结合,而LTP诱导的积累是独立于化.

结论:

基化是维护记忆和突触可塑性的关键机制,特别是LTP诱导.
减少的CaMKII化有助于与年龄相关的认知和突触缺陷.
向CaMKII化可能为与年龄相关的记忆障碍提供治疗策略.

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