The effect of fluoxetine on astrocyte autophagy flux and injured mitochondria clearance in a mouse model of depression
Abstract
Although multiple hypotheses had been proposed to clarify the causes of depression, the accurate pathogenesis and effective treatment of depression still need to be solved. Pathological change of astrocytes has been recognized to play a pivotal role in depression. Fluoxetine is the first selective serotonin reuptake inhibitor, however, the underlying mechanisms of fluoxetine are incompletely excavated. Emerging evidence shows that fluoxetine promotes autophagic processes in tumor cells. However, whether astrocytic autophagy gets involved in the cytoprotection of fluoxetine on astrocytes in depression treatment remains unexplored. Here we prepared chronic mild stress (CMS)-induced mouse model and treated mice with fluoxetine (10 mg/kg) for 4 weeks to determine the correlation between proautophagic effect of fluoxetine and astrocyte protection in depression. Primary hippocampal astrocytes were cultured to investigate the potential mechanism of fluoxetine in regulating astrocyte autophagy. We found that fluoxetine (10 mg/kg) treatment promoted autophagosome formation and increased clearance of injured mitochondria, consequently protected astrocytes in CMS model mice. Fluoxetine (10 μM) could also promote the autophagic flux unbloc...Continue Reading
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