Professor Mitch Voda
08 December 2011
Epigenetic: Hidden Switches
Matt is a history teacher. His twin brother Greg is a drug addict. Growing up in the Boston area, both boys did well in high school: they were strong students in the classroom and decent athletes on the field, and they got along with their peers. Like many young people, the brothers drank the occasional beer, smoked cigarettes and experimented with marijuana. Then, in college, they tried cocaine. For Greg, the experience derailed his life. The questions that have risen from this are: what made Greg so susceptible to the grasps of cocaine- to the point that the drug essentially destroyed his life? And how did his identical twin, who shares the exact same genes, escape a similar fate? And how can exposure to a drug set up some individuals for a lifelong addiction, while others can move past their youthful indiscretions and go on to lead productive lives? These questions, although not new, have lead neuroscientist to begin taking a fresh approach to finding the answers. New findings suggest that experience can contribute to mental illness by adding or removing “epigenetic” marks on chromosomes. These tags are particular chemicals that can influence gene activity without changing the information encoded in the gene.
Studies of mice have shown that chronic cocaine exposure shifts the balance of epigenetic marks on genes in the brain’s reward center. This shift renders the animals more sensitive to the drug’s effects and more prone to becoming addicted. Even a single dose of cocaine can alter the epigenetic landscape of genes in the nucleus accumbens, a part of the reward center. In the absence of drugs, methyl marks predominate, keeping the affected chromatin tightly wound and the gene quiet. Cocaine causes acetyl groups to predominate and chromatin to loosen. Then many genes encoding proteins involved in the pleasurable response to the drug become active.
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