Beware! A study has revealed that individuals, who experience childhood stress and trauma, are at increased risk of depression by permanently changing their Deoxyribonucleic Acid (DNA).
The study focuses on epigenetics - a study of changes in the action of genes caused not by changes in DNA code we inherit from our parents, but instead by molecules that regulate when, where and to what degree our genetic material is activated. The function of transcription factors are specialised proteins that bind to specific DNA sequences in our genes and either encourage or shut down the expression of a given gene. The study’s lead investigator Catherine Pena said that the work identifies a molecular basis for stress during a sensitive developmental window that programs a mouse’s response to stress in adulthood.
“We discovered that disrupting maternal care of mice produces changes in levels of hundreds of genes in the Ventral Tegmental Area (VTA), neurons located close to the midline on the floor of the midbrain, that primes this brain region to be in a depression-like state, even before we detect behavioural changes. Essentially, this brain region encodes a lifelong, latent susceptibility to depression that is revealed only after encountering additional stress,” Peña added. The investigators identified a role for the developmental transcription factor orthodenticle homeobox 2 (Otx2) as a master regulator of these enduring gene changes.
The team showed that baby mice that were stressed in a sensitive period (from postnatal day 10-20) had suppressed Otx2 in the VTA. While Otx2 levels ultimately recovered by adulthood, the suppression had already set in motion gene alterations that lasted into adulthood, indicating that early life stress disrupts age-specific developmental programming orchestrated by Otx2. To test the prediction that Otx2 was actually responsible for the stress sensitivity, the team developed viral tools that were used to either increase or decrease Otx2 levels.
{{/usCountry}}The team showed that baby mice that were stressed in a sensitive period (from postnatal day 10-20) had suppressed Otx2 in the VTA. While Otx2 levels ultimately recovered by adulthood, the suppression had already set in motion gene alterations that lasted into adulthood, indicating that early life stress disrupts age-specific developmental programming orchestrated by Otx2. To test the prediction that Otx2 was actually responsible for the stress sensitivity, the team developed viral tools that were used to either increase or decrease Otx2 levels.
{{/usCountry}}They found that suppression of Otx2 early in life was both necessary and sufficient for increased susceptibility to adult stress. Senior investigator of the study, Eric J. Nestler, said that this mouse paradigm will be useful for understanding the molecular correlates of increased risk of depression resulting from early life stress and could pave the way to look for such sensitive windows in human studies. The study is published in the journal Science.
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