“一朝被蛇咬，十年怕井绳”。人们对经历的刺激会产生恐惧、甚至终生难忘的秘密，近日被复旦大学科学家发现。最近一期的美国《国家科学院院刊》（PNAS）上刊登了这一成果，发表后即被著名《自然》杂志“自然中国”网站列为“研究亮点”，并以“神经科学：恐惧因子”为题作详细报道。
复旦大学脑科学研究院马兰研究组在报告中指出，蛋白质β抑制因子在记忆形成中扮演了至关重要的角色，是一个参与恐惧记忆的“恐怖分子”。他们对老鼠进行了“恐惧记忆”的研究，在播放声音的同时对小鼠进行电击，他们发现，缺失了β抑制因子基因的小鼠难以对声音产生恐惧，即便形成了恐惧记忆，也会比正常的老鼠更快忘记。
报告指出，恐惧能够选择性地激活脑杏仁复合体区域的蛋白激酶A和β抑制因子，β抑制因子对蛋白激酶A神经信号通路的调节、对恐惧记忆形成有关键作用。学界普遍认为，这项成果将有助于给人类因事故、战争或灾难性心理创伤造成的精神障碍等疾病的治疗带来新的希望。
更多阅读
《国家科学院院刊》发表论文摘要（英文）
print December 2, 2009, doi: 10.1073/pnas.0906941106 PNAS December 22, 2009 vol. 106 no. 51 21918-21923
Regulation of amygdalar PKA by β-arrestin-2/phosphodiesterase-4 complex is critical for fear conditioning
Abstract
β-arrestins, key regulators of receptor signaling, are highly expressed in the central nervous system, but their roles in brain physiology are largely unknown. Here we show that β-arrestin-2 is critically involved in the formation of associative fear memory and amygdalar synaptic plasticity. In response to fear conditioning, β-arrestin-2 translocates to amygdalar membrane where it interacts with PDE-4, a cAMP-degrading enzyme, to inhibit PKA activation. Arrb2/ mice exhibit impaired conditioned fear memory and long-term potentiation at the lateral amygdalar synapses. Moreover, expression of the β-arrestin-2 in the lateral amygdala of Arrb2/ mice, but not its mutant form that is incapable of binding PDE-4, restores basal PKA activity and rescues conditioned fear memory. Taken together, our data demonstrate that the feedback regulation of amygdalar PKA activation by β-arrestin-2 and PDE-4 complex is critical for the formation of conditioned fear memory.
