长时程增强
突触可塑性
神经科学
海马结构
新颖性
海马体
变质塑性
心理学
记忆巩固
树突棘
识别记忆
神经可塑性
认知
医学
内科学
社会心理学
受体
作者
Qingyan Jiao,Xi Dong,Cunle Guo,Tongrui Wu,Feng Chen,Kai Zhang,Zengguang Ma,Yukui Zhang,Haiyan Cao,Chao Tian,Qi Hu,Nannan Liu,Yong Wang,Lijie Ji,Shutong Yang,Xin‐Jun Zhang,Jie Li,Hui Shen
标识
DOI:10.1016/j.bbr.2021.113621
摘要
Sleep is essential for important physiological functions. Impairment of learning and memory function caused by lack of sleep is a common physiological phenomenon of which underlying changes in synaptic plasticity in the hippocampus are not well understood. The possible different effects of sleep deprivation (SD) lasting for various durations on learning and memory function and hippocampal synaptic plasticity are still not completely clear. In this study, we used a modified multiple platform method (MMPM) to induce rapid eye movement SD (REM SD), lasting for 24 h, 48 h, and 72 h, separately. The novel place recognition (NPR) and novel object recognition (NOR) tasks were used to test the novelty-related object recognition memory (ORM) and object location memory (OLM) of mice. Then, hippocampal synaptic plasticity was evaluated after all behavioural experiments. The results showed that REM SD played a key role in OLM but not in ORM. Specifically, 24 h REM SD improved novelty-related OLM, accompanied by a significantly increased hippocampal synaptic plasticity, including gain of dendritic spines, increased expression of hippocampal GluA1, and enhanced long-term potentiation (LTP), whereas 48 h REM SD showed no effect on OLM or the hippocampal synaptic plasticity mentioned above; however, 72 h REM SD impaired novelty-related OLM and weakened hippocampal synaptic plasticity, including serious loss of dendritic spines, decreased expression of hippocampal GluA1, and significantly attenuated LTP. Our results suggest that REM SD of various durations has different effects on both novelty-related OLM and hippocampal synaptic plasticity.
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