Sial Omar K, Warren Brandon L, Alcantara Lyonna F, Parise Eric M, Bolaños-Guzmán Carlos A
Department of Psychology and Program in Neuroscience, Florida State University, Tallahassee, FL 32306-4301, United States.
National Institute on Drug Abuse, Behavioral Neuroscience Research Branch, Baltimore, MD, United States.
J Neurosci Methods. 2016 Jan 30;258:94-103. doi: 10.1016/j.jneumeth.2015.10.012. Epub 2015 Nov 3.
Animal models capable of differentiating the neurobiological intricacies between physical and emotional stress are scarce. Current models rely primarily on physical stressors (e.g., chronic unpredictable or mild stress, social defeat, learned helplessness), and neglect the impact of psychological stress alone. This is surprising given extensive evidence that a traumatic event needs not be directly experienced to produce enduring perturbations on an individual's health and psychological well-being. Post-traumatic stress disorder (PTSD), a highly debilitating neuropsychiatric disorder characterized by intense fear of trauma-related stimuli, often occurs in individuals that have only witnessed a traumatic event.
By modifying the chronic social defeat stress (CSDS) paradigm to include a witness component (witnessing the social defeat of another mouse), we demonstrate a novel behavioral paradigm capable of inducing a robust behavioral syndrome reminiscent of PTSD in emotionally stressed adult mice.
We describe the vicarious social defeat stress (VSDS) model that is capable of inducing a host of behavioral deficits that include social avoidance and other depressive- and anxiety-like phenotypes in adult male mice. VSDS exposure induces weight loss and spike in serum corticosterone (CORT) levels. A month after stress, these mice retain the social avoidant phenotype and have an increased CORT response when exposed to subsequent stress.
COMPARISON WITH EXISTING METHOD(S): The VSDS is a novel paradigm capable of inducing emotional stress by isolating physical stress/confrontation in mice.
The VSDS model can be used to study the short- and long-term neurobiological consequences of exposure to emotional stress in mice.
能够区分身体应激和情绪应激之间神经生物学复杂性的动物模型很少见。目前的模型主要依赖于身体应激源（例如，慢性不可预测或轻度应激、社会挫败、习得性无助），而忽视了单独心理应激的影响。鉴于大量证据表明，创伤性事件不一定需要直接经历就能对个体的健康和心理健康产生持久干扰，这一点令人惊讶。创伤后应激障碍（PTSD）是一种高度致残的神经精神疾病，其特征是对与创伤相关的刺激有强烈恐惧，通常发生在仅目睹过创伤性事件的个体中。
通过修改慢性社会挫败应激（CSDS）范式，使其包含一个见证成分（目睹另一只小鼠的社会挫败），我们展示了一种新的行为范式，该范式能够在情绪应激的成年小鼠中诱导出一种强烈的行为综合征，让人联想到创伤后应激障碍。
我们描述了替代性社会挫败应激（VSDS）模型，该模型能够在成年雄性小鼠中诱导出一系列行为缺陷，包括社交回避以及其他类似抑郁和焦虑的表型。VSDS暴露会导致体重减轻和血清皮质酮（CORT）水平飙升。应激一个月后，这些小鼠仍保持社交回避表型，并且在暴露于后续应激时CORT反应增强。
VSDS是一种能够通过在小鼠中分离身体应激/对抗来诱导情绪应激的新范式。
VSDS模型可用于研究小鼠暴露于情绪应激后的短期和长期神经生物学后果。
