Working with mouse cells in the lab, the researchers used microarray technologies to search for genes other than Gabra4 that might be activated when the heat shock pathway was exposed to alcohol. They found many others.
"The big question that remains is how does this activation occur" The current theory holds that, under conditions of stress, heat shock proteins break away from a key molecule, HSF1. HSF1 then makes its way to the cell nucleus, where it helps stimulate the transcription and activation of a variety of genes that enable the cell to survive stress. We think this may happen with alcohol exposure," Dr. Harrison explains.
This finding, observed in vitro in the cell cultures, was replicated in in vivo experiments in mice, conducted in the lab of Dr. Daniel Herrera, assistant professor of psychiatry at Weill Cornell and an attending psychiatrist at NewYork-Presbyterian/Weill Cornell.
"It was really exciting to see this mechanism work itself out in an animal model, suggesting that this same pathway may mediate at least some of the effects of alcohol on human brain cells," Dr. Herrera says.
Exactly what those effects might mean clinically remains in the realm of speculation for now, the researchers stress.
"Alcohol can have bad effects -- the well-known effects of alcoholism, such as liver or brain damage, for example -- but moderate alcohol use also has more benign effects, such as the improvement in cardiovascular health observed in drinkers of red wine com
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| Contact: Andrew Klein ank2017@med.cornell.edu 212-821-0560 New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College Source:Eurekalert |