"We know that genes influence nicotine behaviours, but trying to figure out what specific genetic variants do requires different types of tools," said Helen Kamens, assistant professor of biobehavioural health at Pennsylvania State University.
Nicotine binds to and activates specific receptors on nerve cells in the brain that can also bind the neurotransmitter acetylcholine. These receptors are made up of five subunits, and human genetic studies show that changes in a single subunit can alter nicotine behaviour.
The researchers at Penn State and the University of Colorado focused on the gene that encodes the beta-3 subunit, which is found in areas of the brain important in drug behaviour.
"This work was based on associations that were found in human genetic studies. Genetic variants were shown to affect certain nicotine behaviors, but the question was why? Here we focused on trying to figure out what these genetic variants actually do," Kamens said.
The researchers used a mouse model to study how reducing how much of the beta-3 subunit was made, or preventing its production completely, affected nicotine consumption.
They used genetic engineering techniques to remove one or both copies of the beta-3 gene.
Then, to measure how much the mice wanted the drug, the researchers provided each mouse with two water bottles, one with nicotine and one without nicotine, and recorded how much water the mice drank from each bottle.
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