Numerous studies have alleged that a traumatic experience in our life leaves a scar in our mind. Now a new study from Rockefeller University describes a method by which a stressful experience could alter the way that genes are expressed in the rat brain. The finding of ‘epigenetic’ regulation of genes in the brain is apparently aiding in changing the way scientists believe about psychiatric disorders and could unlock new opportunities to treatment.
It was apparently discovered that a single 30-minute incident of heightened stress may cause a swift chemical change in DNA packaging proteins known as histones in the rat hippocampus, which is a brain area apparently recognized to be particularly vulnerable to the outcomes of stress in both rodents and humans. This was found by Richard Hunter, a postdoc in Rockefeller University’s Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology.
The chemical change was known as methylation and could either augment or reduce the expression of genes that seem to be packaged by the histones, depending on the site of the methylation. Hunter searched for methylation on three areas of histone H3 that have been supposedly demonstrated to vigorously adjust gene expression. He illustrates that methylation of one mark, H3K9 trimethyl, is said to be approximately doubled in the hippocampus. Methylation of a second mark, H3K27 trimethyl, apparently fell by almost 50 percent in the same region. Alterations linked with the third mark were claimed to be negligible.
Richard Hunter who worked on the project with Rockefeller scientists Bruce S. McEwen and Donald W. Pfaff, commented, “The hippocampus is involved in episodic memory, so you would expect it to be sensitive to episodic experiments like this, more so than the motor regions, for instance. But what is surprising is the magnitude and regional specificity of these patterns.â€
Just the size of the change in histone methylation apparently proposes that it appears to be significant to the brain’s response to severe stress, even though its precise function is a mystery. The two methyl marks that altered are both believed to suppress gene expression typically, but methylation apparently augmented in one and reduced in the other.
Hunter also searched for similar modifications as a result of chronic stress exposure to a 30-minute stress every day for around 21 days. Apparently, he did not hit upon a chief effect, which could mirror the animals’ adjusting to the stress. Nevertheless, when he treated the rats with fluoxetine, he apparently reversed some methylation effects linked with chronic stress.
It is supposedly turning out to be progressively more obvious, that the epigenetic changes such as the methyl marks others like acetylation and phosphorylation, could play an important function in the brain’s response to stress and the treatment of stress associated diseases like post-traumatic stress disorder.
The study was published in the Proceedings of the National Academy of Sciences.