Behavioural studies have reported that experimental depression rodent models (corticosterone administration model, chronic unpredictable stress model and acute/chronic restraint stresses models) had a decreased expression of mRNA and Cx43 protein in the frontal cortex, whereas these depression models displayed a contradiction between suppressed gap junction permeability and enhanced hemichannel permeability [33,37,38,39,40,41]. This evidence concerns the gene GJA1 and depressive symptom measurement.