Krawczyk Maria C, Millan Julieta, Blake Mariano G, Feld Mariana, Boccia Mariano M
Laboratorio de Neurofarmacología de los Procesos de Memoria, Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina.
Instituto de Fisiología y Biofísica (IFIBIO UBA-CONICET), Facultad de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina.
Front Mol Neurosci. 2019 Apr 17;12:95. doi: 10.3389/fnmol.2019.00095. eCollection 2019.
Back in 1968, Misanin and his group posited that reactivation of consolidated memories could support changes in that trace, similar to what might happen during the consolidation process. Not until 2000, when Nader et al. (2000) studied the behavioral effect of a protein synthesis inhibitor on retrieved memories, could this previous statement be taken under consideration once again; suggesting that consolidated memories can become labile after reactivation. The process of strengthening after memory labilization was named memory reconsolidation. In recent years, many studies pointed towards a critical participation of the extracellular signal-regulated kinase (ERK)/mitogen activated protein kinases (MAPKs) pathway in different memory processes (e.g., consolidation, extinction, reconsolidation, among others). In this review article, we will focus on how this system might be modulating the processes triggered after retrieval of well-consolidated memories in mice.
早在1968年,米萨宁和他的团队就提出,巩固记忆的重新激活可以支持该记忆痕迹的变化,这类似于巩固过程中可能发生的情况。直到2000年,纳德尔等人(2000年)研究了蛋白质合成抑制剂对提取记忆的行为影响,上述观点才再次被考虑;这表明巩固后的记忆在重新激活后可能会变得不稳定。记忆不稳定后的强化过程被称为记忆再巩固。近年来,许多研究表明细胞外信号调节激酶(ERK)/丝裂原活化蛋白激酶(MAPK)通路在不同的记忆过程(如巩固、消退、再巩固等)中起关键作用。在这篇综述文章中,我们将重点关注该系统如何调节小鼠中巩固良好的记忆提取后触发的过程。