Ravassard Pascal, Hamieh Al Mahdy, Malleret Gaël, Salin Paul-Antoine
Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche 5292, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 1028, France; Physiopathology of the Sleep Neuronal Networks, Lyon Neuroscience Research Center, F-69008 Lyon, France; University Lyon 1, F-69000 Lyon, France.
Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche 5292, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 1028, France; Physiopathology of the Sleep Neuronal Networks, Lyon Neuroscience Research Center, F-69008 Lyon, France; University Lyon 1, F-69000 Lyon, France.
Neurobiol Learn Mem. 2015 Jul;122:4-10. doi: 10.1016/j.nlm.2014.11.013. Epub 2014 Nov 28.
Memory consolidation is the process for long-term storage of information and protection against interferences. It has been proposed that long-term potentiation (LTP), the long-lasting enhancement of synaptic transmission, is a cellular model for memory consolidation. Since consolidation of several forms of memory is facilitated by paradoxical sleep (PS) we ask whether PS modulates the cellular and molecular pathways underlying LTP. The long-lasting form of LTP (L-LTP) is dependent on the activation of transcription factors, enzymatic cascades and the secreted neurotrophin BDNF. By using PS deprivation, immunohistochemistry and quantitative real-time polymerase chain reaction (qPCR), we showed that an increase in PS amount (produced by rebound in PS deprived rats) is able to up-regulate the expression level of transcription factors Zif268 and c-Fos as well as Arc and BDNF in the CA1 and CA3 areas of the hippocampus. Several studies involved these factors in dendritic protein synthesis and in long-term structural changes of synapses underlying L-LTP. The present study together with the work of others (Ribeiro et al., 2002) suggest that by this mechanism, a post-learning increase in PS quantity (post-learning PS window) could convert a transient form of LTP to L-LTP.
记忆巩固是信息长期存储以及抵御干扰的过程。有人提出，长时程增强（LTP），即突触传递的持久增强，是记忆巩固的细胞模型。由于多种形式的记忆巩固受到异相睡眠（PS）的促进，我们探究PS是否调节LTP潜在的细胞和分子途径。LTP的持久形式（L-LTP）依赖于转录因子、酶促级联反应以及分泌的神经营养因子脑源性神经营因子（BDNF）的激活。通过使用PS剥夺、免疫组织化学和定量实时聚合酶链反应（qPCR），我们发现PS量的增加（由PS剥夺大鼠的反弹产生）能够上调海马体CA1和CA3区域中转录因子Zif268和c-Fos以及Arc和BDNF的表达水平。多项研究表明这些因子参与树突蛋白合成以及L-LTP潜在突触的长期结构变化。本研究以及其他研究（Ribeiro等人，2002年）表明，通过这种机制，学习后PS量的增加（学习后PS窗口）可以将LTP的短暂形式转化为L-LTP。
