The need to take in large amounts of nicotine can be altered by manipulating a protein in the brain.
“These findings also point to a promising target for the development of potential anti-smoking therapies,” says study author Paul Kenny of the Scripps Research Institute.
The researchers looked at a gene called CHRNA5 that controls a particular receptor found in the part of the brain that suppresses reward signals. Nicotine stimulates this receptor.
With a normal version of this gene, anything more than a tiny dose of nicotine triggers a message to the brain which says, in effect, 'stop consuming,' AFP explains. Larger doses unleash a sense of repulsion, similar to "bad-tasting food or drink," according to Kenny.
Genetically modified mice missing this receptor craved and consumed far more nicotine. The negative message was never sent, and they just couldn't get enough. The effect could be reversed by boosting levels of the receptor, the study suggests.
About a third of the US population is thought to have a form of the CHRNA5 gene that encourages unbridled nicotine craving.
"Our data probably explain the fact that individuals with this genetic variation have increased vulnerability to developing tobacco addiction," Kenny says. "They are likely to be far less sensitive to the averse properties of the drug, and are thus more likely to acquire a nicotine habit."
The study was published in Nature on Sunday.
Also this week, scientists have genetically engineered mice to have human diabetes – which means that mice can now be tested with human diabetes drugs, rather than mouse versions.
The study could help researchers tweak doses to improve the safety and efficacy of drugs in humans.
Until now, mice with type 1 diabetes had to be given drugs that were slightly different than those given to people, so side effects remained unexplored, or drugs that looked promising in mice could be ineffective when given to humans.
In type 1 diabetes, the body destroys cells in the pancreas that help regulate sugar levels. People who have this must take insulin – a hormone needed to allow sugar to enter cells for energy production – for the rest of their lives.
The disease typically develops due to autoimmune disorders, where the body’s immune system attacks its own tissues. In particular, the pancreas’s islet cells that produce insulin, are mistakenly targeted.
Anti-human CD3 antibodies help immune systems tolerate the islet cells.
In the mice with human diabetes, the anti-CD3 stopped the disease from progressing – providing a testing platform to perfect promising new treatments.
The study was published in Science Translational Medicine yesterday.
Image: lab mouse via Wiki