Bourtchuladze R, Frenguelli B, Blendy J, Cioffi D, Schutz G, Silva A J
Cold Spring Harbor Laboratory, New York 11724.
Cell. 1994 Oct 7;79(1):59-68. doi: 10.1016/0092-8674(94)90400-6.
The cAMP-responsive element-binding protein (CREB) has been implicated in the activation of protein synthesis required for long-term facilitation, a cellular model of memory in Aplysia. Our studies with fear conditioning and with the water maze show that mice with a targeted disruption of the alpha and delta isoforms of CREB are profoundly deficient in long-term memory. In contrast, short-term memory, lasting between 30 and 60 min, is normal. Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation. However, paired-pulse facilitation and posttetanic potentiation are normal. These results implicate CREB-dependent transcription in mammalian long-term memory.
环磷酸腺苷反应元件结合蛋白（CREB）与长期易化所需的蛋白质合成激活有关，长期易化是海兔记忆的一种细胞模型。我们通过恐惧条件反射和水迷宫实验研究发现，CREB的α和δ亚型被靶向破坏的小鼠在长期记忆方面存在严重缺陷。相比之下，持续30至60分钟的短期记忆则正常。与认为长时程增强（LTP）在记忆中起作用的模型一致，来自CREB突变体的海马切片中的LTP在强直刺激后90分钟衰减至基线水平。然而，双脉冲易化和强直后增强是正常的。这些结果表明CREB依赖的转录在哺乳动物长期记忆中起作用。
