在CA1 LTP中的循环节变化是由刺激-抑制平衡的变化和在小鼠中青春期后逆向方向驱动的
Gonzalo Valdivia1, Cristian Moreno1, Kaiwen He1
1Zanvyl Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, MD 21218.
概括
昼夜节律影响海马体的长期增强 (LTP). 激发-抑制 (E/I) 比率的每日波动,而不是内在容量,驱动这些变化. 阿尔茨海默病和衰老模型显示了改变的模式.
科学领域:
- 神经科学是一个神经科学.
- 时间生物学 时间生物学
- 突触性可塑性 突触性可塑性
背景情况:
- 长期增强 (LTP) 对学习和记忆至关重要.
- 循环节律显著调节突触可塑性,包括LTP.
- 之前的研究表明,在夜间动物的黑暗阶段,LTP更强.
研究的目的:
- 调查CA3-CA1突触中LTP的昼夜调节背后的机制.
- 确定激发-抑制 (E/I) 比在每日LTP波动中的作用.
- 在阿尔茨海默氏症模型和整个发育过程中检查昼夜E/I比率和LTP模式.
主要方法:
- 在小鼠海马片中的电生理学记录.
- 甲爆刺激 (TBS) 和低频刺激 (LFS) 诱导LTP和LTD.
- 对突触抑制的药理学操纵.
- 在不同年龄的野生型 (WT) 和APP/PS1小鼠中进行评估.
主要成果:
- 对于LTP诱导的能力在明暗阶段之间没有差异.
- 甲爆刺激诱导的LTP (TBS-LTP) 幅度与E/I比率相关,在黑暗阶段更高.
- 低频刺激诱导的LTD显示没有昼夜变化.
- 抑制的阻断消除了TBS-LTP的明暗差异.
- APP/PS1小鼠在E/I比率或TBS-LTP中没有每日变化.
- 在青春期之后,WT小鼠在LTP振荡方向上呈现出发育转换.
结论:
- 在E/I平衡中的每日振荡,而不是内在的突触容量,驱动海马体LTP的昼夜调节.
- 这种E/I驱动的昼夜调节在阿尔茨海默病模型中被破坏.
- 在青春期后,这些振荡的发展方向发生了转变,这表明了年龄相关的重组.
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