Region-Dependent Alterations in Cognitive Function and ERK1/2 Signaling in the PFC in Rats after Social Defeat Stress

前额叶皮质 奶油 认知灵活性 心理学 社会失败 神经科学 眶额皮质 脑源性神经营养因子 MAPK/ERK通路 环腺苷酸反应元件结合蛋白 信号转导 单胺类 认知 神经营养因子 内分泌学 内科学 受体 医学 化学 转录因子 生物 血清素 细胞生物学 基因 生物化学
作者
Qiong Wang,Feng Shao,Weiwen Wang
出处
期刊:Neural Plasticity [Hindawi Limited]
卷期号:2018: 1-11 被引量:18
标识
DOI:10.1155/2018/9870985
摘要

Cognitive dysfunctions are highly comorbid with depression. Impairments of cognitive flexibility, which are modulated by the monoaminergic system of the prefrontal cortex (PFC), are increasingly recognized as an important component of the pathophysiology and treatment of depression. However, the downstream molecular mechanisms remain unclear. Using a classical model of depression, this study investigated the effects of social defeat stress on emotional behaviors, on cognitive flexibility in the attentional set-shifting task (AST), and on the expression of extracellular signal-regulated kinase 1 and 2 (ERK1 and ERK2) and their downstream signaling molecules cAMP-response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in two subregions of the PFC, the medial prefrontal cortex (mPFC), and the orbitofrontal cortex (OFC). The results showed that stress induced emotional and cognitive alterations associated with depression, including a decreased sucrose intake ratio and impaired reversal learning and set-shifting performance in the AST. Additionally, rats in the stress group showed a significant decrease only in ERK2 signaling in the mPFC, while more extensive decreases in both ERK1 signaling and ERK2 signaling were observed in the OFC. Along with the decreased ERK signaling, compared to controls, stressed rats showed downregulation of CREB phosphorylation and BDNF expression in both the OFC and the mPFC. Further analysis showed that behavioral changes were differentially correlated with several molecules in subregions of the PFC. These results suggested that social defeat stress was an effective animal model to induce both emotional and cognitive symptoms of depression and that the dysfunction of ERK signaling activities in the PFC might be a potential underlying biological mechanism.
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