Seeking therapeutic targets and molecular signature of major depressive disorder

抄録

According to the World Health Organization, depression is the worldwide concerned issue. It has been estimated that more than 300 million people of all ages suffer from depression. However, the plausible etiological factors of depression are poorly understood. Recent studies have highlighted that the membranes of collapsin response mediator proteins (CRMPs) family are involved in the pathogenesis of various neuropsychiatric disorders, such as schizophrenia, bipolar disorders, and severe major depression. Thus, we examined whether CRMPs family would participate in regulating stress-induced depressive-like behaviors. Herein, we used chronic mild stress (CMS) and social defeat to establish animal models of depression in C57/B6 mice. We found that CMS-treated and social defeated mice exhibited behavioral deficits, many of which were reminiscent of neural features and symptoms associated with depression, when compared to non-stress-treated control mice. Additionally, CMS-treated mice displayed impairments of social interaction and social recognition memory and even in hippocampal-dependent spatial memory loss. Using reverse transcription-PCR (RT-PCR) to quantify the gene expressions of CRMPs family, we found that only hippocampal Crmp5 mRNA levels were significantly lower in the two stress-induced depression models than that of control mice. Our findings revealed that CRMP5 would be a critical role in depressive disorders and could participate in pathways that can be rationally engaged for therapeutic benefit.