The current dogma suggests that the formation of long-term memory (LTM) is dependent on protein synthesis but persistence of the memory trace is not. However, many of the studies examining the effect of protein synthesis inhibitors (PSIs) on LTM persistence were performed in the hippocampus, which is known to have a time-dependent role in memory storage, rather than the cortex, which is considered to be the main structure to store long-term memories. Here we studied the effect of PSIs on LTM formation and persistence in male Wistar Hola (n⩾5) rats by infusing the protein synthesis inhibitor, anisomycin (100 μg, 1 μl), into the gustatory cortex (GC) during LTM formation and persistence in conditioned taste aversion (CTA). We found that local anisomycin infusion to the GC before memory acquisition impaired LTM formation (P=8.9E−5), but had no effect on LTM persistence when infused 3 days post acquisition (P=0.94). However, when we extended the time interval between treatment with anisomycin and testing from 3 days to 14 days, LTM persistence was enhanced (P=0.01). The enhancement was on the background of stable and non-declining memory, and was not recapitulated by another amnesic agent, APV (10 μg, 1 μl), an N-methyl-D-aspartate receptor antagonist (P=0.54). In conclusion, CTA LTM remains sensitive to the action of PSIs in the GC even 3 days following memory acquisition. This sensitivity is differentially expressed between the formation and persistence of LTM, suggesting that increased cortical protein synthesis promotes LTM formation, whereas decreased protein synthesis promotes LTM persistence.

目前的教条表明，长期记忆（LTM）的形成依赖于蛋白质合成，但记忆痕迹的持久性则不然。然而，许多检验蛋白质合成抑制剂 (PSI) 对 LTM 持久性影响的研究是在海马体中进行的，海马体在记忆存储中具有时间依赖性作用，而不是被认为是大脑皮层的皮层。存储长期记忆的主要结构。在这里，我们研究了 PSI 对雄性 Wistar Hola ( n ⩾5) 大鼠通过在 LTM 形成和条件性味觉厌恶 (CTA) 持续期间将蛋白质合成抑制剂茴香霉素 (100 μg, 1 μl) 注入味觉皮层 (GC)。我们发现在记忆获得前向 GC 局部输注茴香霉素会损害 LTM 形成（P = 8.9E-5），但在获得记忆后 3 天输注时对 LTM 持久性没有影响（P = 0.94）。然而，当我们将茴香霉素治疗和测试之间的时间间隔从 3 天延长到 14 天时，LTM 持续性增强（P = 0.01）。这种增强是在稳定且不衰退的记忆的背景下进行的，并且没有被另一种健忘剂 APV（10 μg，1 μl）、一种N-甲基-D-天冬氨酸受体拮抗剂（P = 0.54）。总之，即使在内存获取后 3 天，CTA LTM 仍然对 GC 中 PSI 的作用敏感。这种敏感性在 LTM 的形成和持久性之间存在差异，表明皮质蛋白合成增加促进 LTM 形成，而蛋白质合成减少促进 LTM 持久性。