A previously dismissed genetic mechanism may contribute to nicotine dependence, and to the withdrawal effects that can make quitting smoking difficult, researchers at the University of Michigan (UM) Life Sciences Institute found. 

UM researcher examined withdrawal responses in the millimeter-long roundworms Caenorhabditis elegans, which get hooked on nicotine just like humans, and discovered that a series of genes were involved in a process that ultimately increased the production of the nicotine receptor proteins, with microRNAs, a class of small RNA molecules that help fine-tune gene expression, playing a pivotal role. 

"We're seeing a clear link between nicotine, microRNA, the receptor proteins, and nicotine-dependent behavior," said Jianke Gong, one of the lead authors on the study. 

The findings have provided clues that may carry over to the mammalian realm, and may lead other scientists to re-examine the role of these microRNAs in nicotine dependence in mammals. 

"We have better tools now. We, as a field, need to take another look at this mechanism in nicotine addiction," said Shawn Xu, professor of the Department of Molecular and Integrative Physiology at the UM Medical School. 

The findings have been published in Cell Reports.

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