Increasing evidence has shown that adult hippocampal neurogenesis is closely related to the pathophysiological condition of depressive disorders. Recently, chronic social defeat stress paradigms have been regarded as important animal models of depression, accompanied with neural plastic changes in the hippocampus. However, little is known about influences of non-physical stress on neurogenesis. In the present study, we focused on the chronic vicarious social defeat stress paradigm and examined the effect of psychological stress on mouse hippocampal neurogenesis. Immediately after the chronic psychological stress, the cell survival rate in the dentate gyrus of the hippocampus was significantly diminished without modifying the cell proliferation rate. The decreased ratio in cell survival persisted for 4 weeks after the stress-loading period, while the differentiation and maturity of new-born neurons were identical to control groups. Furthermore, treatment with the chronic antidepressant fluoxetine reversed the social behavioral deficits and promoted new-born neurons survival. These results demonstrate that emotional stress in the vicarious social defeat stress paradigm influences neuronal cell survival in the hippocampus, which reinforces its validity as an animal model of depression.

越来越多的证据表明，成人海马神经发生与抑郁症的病理生理状况密切相关。最近，慢性社会失败压力范式被认为是抑郁症的重要动物模型，伴随着海马的神经可塑性变化。然而，关于非身体压力对神经发生的影响知之甚少。在本研究中，我们专注于慢性替代性社会失败压力范式，并检查了心理压力对小鼠海马神经发生的影响。在慢性心理压力之后，海马齿状回的细胞存活率立即显着降低，而细胞增殖率没有改变。在应激负荷期后，细胞存活率的下降持续了 4 周，而新生神经元的分化和成熟与对照组相同。此外，慢性抗抑郁药氟西汀治疗逆转了社会行为缺陷并促进了新生神经元的存活。这些结果表明，替代性社会失败压力范式中的情绪压力会影响海马神经元细胞的存活，这加强了其作为抑郁症动物模型的有效性。