Neuroscience
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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. ⋯ 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.
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Previous studies have indicated that sex hormones such as prolactin, estradiol and testosterone may play a role in the modulation of adult hippocampal neurogenesis (AHN) in rodents and non-human primates, but so far there has been no investigation of their impact on human hippocampal neurogenesis. Here, we quantify the expression levels of the relevant receptors in human post-mortem hippocampal tissue and a human hippocampal progenitor cell (HPC) line. Secondly, we investigate how these hormones modulate hippocampal neurogenesis using a human in vitro cellular model. ⋯ At this timepoint we instead observe a decrease in proliferation. Overall, our study demonstrates relatively minor, and possibly short-term effects of sex hormones on hippocampal neurogenesis in human cells. Further work will be needed to understand if our results differ to previous animal research due to species-specific differences, or whether it relates to limitations of our in vitro model.