Instituto de Biología Celular y Neurociencias, Facultad de Medicina, UBA, Paraguay 2155 3rd floor, 1121, Buenos Aires, Argentina.
Neurotox Res. 2010 Nov;18(3-4):377-85. doi: 10.1007/s12640-010-9155-5. Epub 2010 Feb 12.
Although much is known about long-term memory (LTM) consolidation, what puts the "long" in LTM is the exclusive feature of persisting over time. However, until recently the molecular mechanisms underneath memory persistence had never been properly studied. In rats, the protein translation inhibitor anisomycin impaired memory persistence when injected into the dorsal hippocampus 12 h after inhibitory avoidance (IA) training without affecting memory formation. Here, we also show learning-induced changes in hippocampal c-Fos, Homer 1a, Akt, CamKIIα, and ERK2 levels around 18-24 h after IA training. Thus, memory persistence is associated with a late phase of plasticity-related protein synthesis in the hippocampus.
尽管人们对长期记忆（LTM）的巩固有了很多了解，但使 LTM 具有“长期”特征的是其随时间持续存在的独特特性。然而，直到最近，记忆持久性背后的分子机制还从未得到过适当的研究。在大鼠中，蛋白翻译抑制剂anisomycin 在抑制性回避（IA）训练后 12 小时注入背侧海马体时会损害记忆持久性，而不会影响记忆形成。在这里，我们还显示了 IA 训练后 18-24 小时海马体中 c-Fos、 Homer1a、Akt、CamKIIα 和 ERK2 水平的学习诱导变化。因此，记忆持久性与海马体中与可塑性相关的蛋白质合成的后期阶段有关。
