Mice selectively bred for High and Low fear behavior show differences in the number of pMAPK (p44/42 ERK) expressing neurons in lateral amygdala following Pavlovian fear conditioning.
Mice selectively bred for High and Low fear behavior show differences in the number of pMAPK (p44/42 ERK) expressing neurons in lateral amygdala following Pavlovian fear conditioning.
复制标题
选择性培育高恐惧行为和低恐惧行为的小鼠在巴甫洛夫恐惧条件反射后，外侧杏仁核中表达 pMAPK (p44/42 ERK) 的神经元数量存在差异。
DOI：
10.1016/j.nlm.2013.06.010
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发表时间：
2014
影响因子：
2.7
通讯作者：
Johnson,LukeR
中科院分区：
文献类型：
--
作者：
Coyner,Jennifer;McGuire,JenniferL;Parker,ClarissaC;Ursano,RobertJ;Palmer,AbrahamA;Johnson,LukeR
条件性恐惧的获得、巩固和消退过程中的个体差异可能会导致包括创伤后应激障碍（PTSD）在内的恐惧病理学的发展。巴甫洛夫恐惧条件反射是研究恐惧学习基本方面的关键工具。在这里，我们使用了一个选择的高和低巴甫洛夫条件恐惧的小鼠线创建一个先进的杂交线（AIL），以开始，以确定巴甫洛夫恐惧条件反射的表型分歧的细胞基础。我们研究了是否磷酸化MAPK（p44/42 ERK/MAPK），蛋白激酶所需的杏仁核的收购和巩固巴甫洛夫恐惧记忆，差异表达巴甫洛夫恐惧学习后，在高和低恐惧线。我们发现，以下巴甫洛夫听觉恐惧条件反射，高和低线小鼠不同的pMAPK表达的神经元在背侧杏仁核（LAd）的数量。相反，这种差异没有检测到腹内侧（LAvm）或腹外侧（LAvl）杏仁核亚核或对照组动物。我们认为，恐惧记忆获得和巩固已知位点的可塑性明显增加与两种恐惧表型之间的内在差异有关。这些数据为理解编码恐惧表型差异的微网络机制提供了重要的见解。了解回路水平的细胞和分子机制，这些机制是恐惧学习中个体差异的基础，对于开发有效治疗与恐惧相关的疾病（如PTSD）至关重要。
Individual variability in the acquisition, consolidation and extinction of conditioned fear potentially contributes to the development of fear pathology including posttraumatic stress disorder (PTSD). Pavlovian fear conditioning is a key tool for the study of fundamental aspects of fear learning. Here, we used a selected mouse line of High and Low Pavlovian conditioned fear created from an advanced intercrossed line (AIL) in order to begin to identify the cellular basis of phenotypic divergence in Pavlovian fear conditioning. We investigated whether phosphorylated MAPK (p44/42 ERK/MAPK), a protein kinase required in the amygdala for the acquisition and consolidation of Pavlovian fear memory, is differentially expressed following Pavlovian fear learning in the High and Low fear lines. We found that following Pavlovian auditory fear conditioning, High and Low line mice differ in the number of pMAPK-expressing neurons in the dorsal sub nucleus of the lateral amygdala (LAd). In contrast, this difference was not detected in the ventral medial (LAvm) or ventral lateral (LAvl) amygdala sub nuclei or in control animals. We propose that this apparent increase in plasticity at a known locus of fear memory acquisition and consolidation relates to intrinsic differences between the two fear phenotypes. These data provide important insights into the micronetwork mechanisms encoding phenotypic differences in fear. Understanding the circuit level cellular and molecular mechanisms that underlie individual variability in fear learning is critical for the development of effective treatment of fear-related illnesses such as PTSD.