创伤后应激障碍（PTSD）是典型的精神刺激所致精神损伤之一。恐惧记忆过度泛化是PTSD发病易感性与慢性化的发生基础。伏隔核（Nac）为杏仁体、海马谷氨酸能神经信号的汇聚、分离及整合脑区，对情绪记忆巩固具有调节作用。研究表明强烈厌恶性应激与糖皮质激素，可增强动物的条件性恐惧记忆泛化。因此，我们假设杏仁体-海马通路糖皮质激素受体（GR）系统与Nac多巴胺（DA）能信号系统可能参与了恐惧记忆特异性向过度泛化的转变，而Nac在神经信息整合过程中具有“开关”作用。本项目将围绕PTSD恐惧记忆过度泛化这一特征性认知行为，验证Nac对恐惧记忆泛化形成的“开关”作用，获得中脑DA神经元位相性兴奋与外周DA水平变化特征，明确Nac中心核-壳核通路DA能神经信息加工机制，探索GR对Nac DA能信号系统的调控机制，阐明Nac对恐惧记忆泛化形成发挥“开关”作用的发生机制，为精神损伤客观评定提供科学依据。

Post-traumatic stress disorder (PTSD) is one of the typical mental injury. Fear memories overgeneralization results in susceptibility and chronicity of PTSD. Nucleus accumbens (Nac) play a key role in convergence, segregation, and interaction of glutamatergic inputs from basolateral amygdala (BLA) and hippocampus (HPC), has important effects on emotional memory consolidation. Studies have shown that intensive stress and glucocorticoids (GCs), may enhance animal generalization of conditioned fear memory. Therefore, we assume that GCs receptor (GR) system in BLA-HPC circuit and Nac dopamine (DA) signaling pathway may be involved in the switch from specific to overgeneralized fear memory, and Nac has a ‘switch’ role in the information integration. This project will focus on PTSD characteristic fear memory overgeneralization, verify the ‘switch’ role of Nac in generalization of fear memory, investigates neuron phasic dopamine release and DA level of midbrain, clarify the dopaminergic information processing mechanism of Nac core-shell circuit, and explore DA-GR interactions in mediating for Nac ‘switch’ signaling mechanism in generalized fear memory formation in order to provide a scientific basis of objective assessment of mental injury.