First, behavioral geneticists at the University of Colorado compared the average daily nicotine consumption in mice. Co-author Jerry Stitzel, PhD, and his team found that mice with the "threonine" polymorphism (an alteration to a gene's DNA sequence) in a gene called Chrna4 consumed significantly more nicotine than mice with an alanine polymorphism in the same gene. The authors think that this threonine variation may allow these mice to tolerate higher nicotine levels before experiencing negative nervous-system side effects.
Chrna4 (Cholinergic Receptor Nicotinic Alpha4) contains the instructions to build a protein that is part of a receptor that recognizes acetylcholine, a major neurotransmitter that plays a role in the brain's pleasure system and also aids learning and memory, sleep, control of muscle movement, heart rate, blood pressure and more. Because nicotine is chemically very similar to acetylcholine, it binds to the same receptors, including those with the protein made from Chrna4. Thus the nervous system responds to nicotine as if it were acetylcholine.
The authors conclude that natural variations in Chrna4 could, by varying how the nicotine receptors works, result in animal-by-animal variation in nicotine tolerance. That may explain why in humans (the gene is found in essentially all animals), CHRNA4 polymorphisms are associated with nicotine dependence. People with certain gene variations may be able to tolerate more nicotine before they get sick and as a result smoke more in the first place, promoting addiction. Nicotine is a natural insecticide found only in tobacco. Like other insecticides, it is ex
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