Scientists have identified a genetic pathway that contributes to nicotine addiction and makes it difficult for smokers to kick the butt. Researchers at the University of Michigan in the US examined withdrawal responses in the millimeter-long roundworms called Caenorhabditis elegans, which get hooked on nicotine just like humans.
The study, published in the journal Cell Reports, identified specific genes and microRNA that play an essential role in how the roundworms develop nicotine dependence and withdrawal responses – clues that may carry over to the mammalian realm.
The study took a fresh look at a previously dismissed biological mechanism. Most research in the field has focused on how proteins called nicotine acetylcholine receptors contribute to dependence. Researchers focused on an earlier step in the genetic coding process 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 behaviour,” said Jianke Gong, a researcher at the University of Michigan. This mechanism had been dismissed as unimportant to nicotine dependence. However, those conclusions were made decades ago, using less sophisticated techniques, researchers said. The discovery in C elegans will now lead other scientists to re-examine the role of these microRNAs in nicotine dependence in mammals, and ultimately lead to a better understanding of what causes the dependence, researchers said.
“People believed this question had been settled,” said Shawn Xu, a professor at the University of Michigan. “But we have better tools now. We, as a field, need to take another look at this mechanism in nicotine addiction,” said Xu.
The study, published in the journal Cell Reports, identified specific genes and microRNA that play an essential role in how the roundworms develop nicotine dependence and withdrawal responses – clues that may carry over to the mammalian realm.
The study took a fresh look at a previously dismissed biological mechanism. Most research in the field has focused on how proteins called nicotine acetylcholine receptors contribute to dependence. Researchers focused on an earlier step in the genetic coding process 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 behaviour,” said Jianke Gong, a researcher at the University of Michigan. This mechanism had been dismissed as unimportant to nicotine dependence. However, those conclusions were made decades ago, using less sophisticated techniques, researchers said. The discovery in C elegans will now lead other scientists to re-examine the role of these microRNAs in nicotine dependence in mammals, and ultimately lead to a better understanding of what causes the dependence, researchers said.
“People believed this question had been settled,” said Shawn Xu, a professor at the University of Michigan. “But we have better tools now. We, as a field, need to take another look at this mechanism in nicotine addiction,” said Xu.