Department of Psychiatry and Program in Neuroscience, School of Medicine, Uniformed Services University (USU), Bethesda, MD, USA.
Eur J Neurosci. 2013 Nov;38(9):3314-24. doi: 10.1111/ejn.12337. Epub 2013 Aug 22.
Genetic variability in the strength and precision of fear memory is hypothesised to contribute to the etiology of anxiety disorders, including post-traumatic stress disorder. We generated fear-susceptible (F-S) or fear-resistant (F-R) phenotypes from an F8 advanced intercross line (AIL) of C57BL/6J and DBA/2J inbred mice by selective breeding. We identified specific traits underlying individual variability in Pavlovian conditioned fear learning and memory. Offspring of selected lines differed in the acquisition of conditioned fear. Furthermore, F-S mice showed greater cued fear memory and generalised fear in response to a novel context than F-R mice. F-S mice showed greater basal corticosterone levels and hypothalamic corticotrophin-releasing hormone (CRH) mRNA levels than F-R mice, consistent with higher hypothalamic-pituitary-adrenal (HPA) axis drive. Hypothalamic mineralocorticoid receptor and CRH receptor 1 mRNA levels were decreased in F-S mice as compared with F-R mice. Manganese-enhanced magnetic resonance imaging (MEMRI) was used to investigate basal levels of brain activity. MEMRI identified a pattern of increased brain activity in F-S mice that was driven primarily by the hippocampus and amygdala, indicating excessive limbic circuit activity in F-S mice as compared with F-R mice. Thus, selection pressure applied to the AIL population leads to the accumulation of heritable trait-relevant characteristics within each line, whereas non-behaviorally relevant traits remain distributed. Selected lines therefore minimise false-positive associations between behavioral phenotypes and physiology. We demonstrate that intrinsic differences in HPA axis function and limbic excitability contribute to phenotypic differences in the acquisition and consolidation of associative fear memory. Identification of system-wide traits predisposing to variability in fear memory may help in the direction of more targeted and efficacious treatments for fear-related pathology.
遗传变异在恐惧记忆的强度和准确性方面被假设为导致焦虑障碍的病因,包括创伤后应激障碍。我们通过选择性繁殖,从 C57BL/6J 和 DBA/2J 近交系的 F8 高级互交系(AIL)中产生了恐惧易感(F-S)或恐惧抗性(F-R)表型。我们确定了个体在条件性恐惧学习和记忆中变异性的特定特征。选择线的后代在条件性恐惧的获得中存在差异。此外,与 F-R 小鼠相比,F-S 小鼠在对新环境的条件性恐惧记忆和泛化恐惧方面表现出更大的恐惧。F-S 小鼠的基础皮质酮水平和下丘脑促肾上腺皮质激素释放激素(CRH)mRNA 水平高于 F-R 小鼠,与更高的下丘脑-垂体-肾上腺(HPA)轴驱动一致。与 F-R 小鼠相比,F-S 小鼠的下丘脑盐皮质激素受体和 CRH 受体 1 mRNA 水平降低。锰增强磁共振成像(MEMRI)用于研究大脑活动的基础水平。MEMRI 鉴定了 F-S 小鼠大脑活动增加的模式,该模式主要由海马体和杏仁核驱动,表明 F-S 小鼠的边缘回路活动过度,与 F-R 小鼠相比。因此,施加于 AIL 群体的选择压力导致每个系内遗传相关特征的积累,而与行为无关的特征仍然分布。因此,选择的系最大限度地减少了行为表型和生理学之间的假阳性关联。我们证明,HPA 轴功能和边缘兴奋性的内在差异导致了联想性恐惧记忆的获得和巩固方面的表型差异。确定导致恐惧记忆变异性的系统范围特征可能有助于更有针对性和有效的针对与恐惧相关的病理学的治疗。