海马体的CaMKII抑制诱导了对灭绝记忆的反应依赖性失忆症,并导致恐惧复发
Andressa Radiske1,2,3, Carla Miranda de Castro1, Janine I Rossato1,4
1Memory Research Laboratory - Brain Institute, Federal University of Rio Grande do Norte, Natal, RN, Brazil.
Scientific reports
|December 8, 2023
概括
海马体CaMKII对于稳定恐惧灭绝记忆再巩固至关重要. 在回忆后抑制CaMKII会破坏这个过程,导致恐惧恢复.
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
- 行为科学 行为科学
背景情况:
- 恐惧灭绝记忆需要由大脑衍生的神经营养因子 (BDNF) 相关的再巩固.
- Ca2+/calmodulin依赖蛋白激酶II (CaMKII) 对于记忆处理至关重要,作用于GluN2B-NMDAR的下游,并影响BDNF的表达.
研究的目的:
- 研究海马CaMKII在恐惧灭绝记忆再巩固中的作用.
- 为了确定CaMKII活动是否对于灭绝记忆的持久性是必要的.
主要方法:
- 使用了成年雄性Wistar大鼠.
- 在海马体的背部CA1区域中对CaMKII的药理抑制.
- 使用了行为恐惧灭绝和回忆范式.
主要成果:
- 内CA1 CaMKII 抑制剂 (AIP,KN-93) 的使用损害了恐惧灭绝记忆的回忆.
- 对CaMKII的抑制导致恐惧的恢复,依赖于GluN2B-NMDAR.
- 不活性类型 (加密AIP,KN-92) 没有产生这些效应.
结论:
- 海马体CaMKII对于恐惧灭绝记忆的重新巩固至关重要.
- 在记忆回忆过程中调节CaMKII活动会影响恐惧抑制的持续性.
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