Viosca Jose, Lopez de Armentia Mikel, Jancic Dragana, Barco Angel
Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas, Sant Joan d'Alacant, 03550 Alicante, Spain.
Learn Mem. 2009 Feb 23;16(3):193-7. doi: 10.1101/lm.1254209. Print 2009 Mar.
Regulated expression of a constitutively active form of cAMP response element-binding protein (CREB), VP16-CREB, lowers the threshold for the late phase of long-term potentiation in the Schaffer collateral pathway in a de novo gene expression-independent manner, and increases the excitability and reduces afterhyperpolarization of neurons at the amygdala and the hippocampus. We explore the consequences of these changes on the consolidation of fear conditioning and find that the expression of VP16-CREB can bypass the requirement for de novo gene expression associated with long-term memory formation, suggesting that CREB-dependent gene expression is sufficient for fear memory consolidation.
组成型活性形式的环磷酸腺苷反应元件结合蛋白（CREB），即VP16-CREB的调控表达，以一种不依赖于从头基因表达的方式降低了海马体中Schaffer侧支通路的长时程增强晚期的阈值，并增加了杏仁核和海马体中神经元的兴奋性，减少了其动作后超极化。我们探究了这些变化对恐惧条件反射巩固的影响，发现VP16-CREB的表达可以绕过与长期记忆形成相关的从头基因表达的需求，这表明依赖CREB的基因表达足以巩固恐惧记忆。
