The hippocampus-prefrontal cortex circuit plays a major role in stress and in the neurobiology of depression and its treatment. Disruption of this circuit by lesioning the thalamic nucleus reuniens (RE) has been shown to prevent the detrimental effects of chronic mild stress on prefrontal cortex neuroplasticity indices in male rats. However, it remains unknown whether hippocampal neurostructural response to stress is modified by RE lesion. In the present study, adult male rats were subjected to the chronic mild stress model of depression and were treated with either vehicle or the antidepressant, sertraline. Moreover, a group of animals was subjected to RE lesion before stress exposure with or without sertraline treatment. We demonstrated that chronic mild stress induced hippocampal CA1 dendritic atrophy and this was prevented by pre-stress RE lesion to the same extent that antidepressant treatment reversed it. The present findings highlight the importance of hippocampal-prefrontal cortex communication in chronic stress effects on hippocampal neuroplasticity and contribute to the elucidation of the role of RE in neurostructural changes underlying stress-driven depression and its treatment.

海马-前额叶皮层回路在压力，抑郁症的神经生物学及其治疗中起主要作用。通过损伤丘脑核（RE）破坏该回路已显示可预防慢性轻度应激对雄性大鼠前额叶皮层神经可塑性指标的有害影响。然而，RE病变能否改变海马对应激的神经结构反应。在本研究中，成年雄性大鼠经历了慢性轻度抑郁症的抑郁模型，并用赋形剂或抗抑郁药舍曲林治疗。此外，在有或没有舍曲林治疗的应激暴露之前，对一组动物进行RE损伤。我们证明了慢性轻度应激会诱发海马CA1树突状萎缩，而应激前RE病变可以预防这种情况，抗抑郁药可以逆转这种程度。本研究结果突出了海马-前额叶皮层通讯在慢性应激对海马神经可塑性的影响中的重要性，并有助于阐明RE在应激驱动性抑郁症及其治疗的神经结构变化中的作用。