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The addition of HDAC2i (an HDAC2 inhibitor) leads to an improvement of depression symptoms in animal model systems. Furthermore, mice with a dominant negative HDAC2 mutation, which suppresses HDAC2 enzymatic activity, generally show less depressive behavior than mice who do not have this dominant negative mutation. This increase in depressive behavior is thought to be caused by HDAC2 target having antidepressant properties, while targets of HDAC5 have depressant properties.

Another study found that HDAC3 was decreased in individuals resilient to depression.

Major depressive disorder is heavily influenced by environmental and genetic factors. These factors include epigenetic modification of the genome in which there is a persistent change in gene expression without a change in the actual DNA sequence. MDD is heavily influenced by environmental and genetic factors. These factors include epigenetic modification of the genome in which there is a persistent change in gene expression without a change in the actual DNA sequence. Genetic and environmental factors can influence the genome throughout a life; however, an individual is most susceptible during childhood. Early life stresses that could lead to MDD include periodic maternal separation, child abuse, divorce, and loss. These factors can result in epigenetic marks that can alter gene expression and impact the development of key brain regions such as the hippocampus. Epigenetic factors, such as methylation, could serve as predictors for the effectiveness of certain antidepressant treatments. Currently, antidepressants can be used to stabilize moods and decrease global DNA methylation levels, but they could also be used to determine the risk of depression caused by epigenetic changes. Identifying gene with altered expression could result in new antidepressant treatments. Depolarization of neurons causing an increase in calcium leads to the phosphorylation of MeCP2, which results in a decrease in the binding of MeCP2 to BDNF promoter IV.