The Eph receptor A4-mediated demyelination in depression

Abstract

Accumulating evidence reveals that major depressive disorder, one of the most common mental illnesses, is characterized by abnormal myelination. However, the relationship between demyelination and depression-related behaviors and the molecular mechanism underlying demyelination and synaptic deficits in depression is largely unknown. In a recent study, Li and his colleagues found that the ephrin A4 receptor (EphA4), a member of the Eph family of receptor tyrosine kinases, was essential to mediate demyelination and regulate synaptogenesis in depression. Using the chronic, unpredictable mild stress (CUMS) exposure or lipopolysaccharide (LPS) administration-induced animal model of depression, the authors found that depression could induce demyelination, and the increased EphA4 levels mediate demyelination and depression-like behaviors. In this commentary, we reviewed this critical finding and discussed future directions on this topic.

Keywords: Depression, Eph receptor A4, demyelination