New scientific find may help smokers quit
In a study that may hold insights into ways to help people quit smoking, researchers at the CNRS-Pasteur Institute in Paris showed that receptors on cells in the ventral tegmental area (VTA) of the brain are involved in nicotine's addictive and cognitive qualities in mice.They think this research could lead to a way to help smokers quit. But I ask you: how? By giving people learning disabilities?
[...]
Changeux and his team genetically engineered mice so they lacked a gene for a portion of a nicotine receptor, to discover the impact it would have on how the mice functioned.
The mutant mice had a mild learning impairment and unlike normal mice, which had learned to press a lever to self-administer nicotine, they showed no interest in getting nicotine.
"When there is a loss of the nicotine receptor then there is a loss of cognitive function in the mouse," Changeux, who reported the finding in the science journal Nature, told Reuters.
But when the scientists re-injected the gene, the mice's cognitive function was restored. The rodents were also more likely to seek out nicotine.
I mean, really; is this article just horribly written? Obviously it is--just try and interpret the first sentence. But is it so horribly written that important facts vital to comprehension of the meaning of this study are omitted? Or am I missing something?
If cognitive function and nicotine receptors are inextricably linked, what does this mean? Is cognitive function affected by whether or not a person smokes, or only by whether or not they have nicotine receptors? And what do they mean by "mild learning impairment"? How mild, exactly? I don't smoke, so this is all academic, but if I did, I can't imagine that any level of "learning impairment" would be acceptable to me.
4 comments:
all this talk has made me want to smoke more
LOL!
Well, let me know if smoking helps you understand the article o_o
Clearly smoking is so bad that we smokers should be made stupid in order to help us do something smart!
I figured that out on a smoke break, so it seems that smoking did help me understand the article.
I'm assuming that they are using the term learning disability in the same way researchers used it in a similar story about addicition to pain killers. Every medicine/chemical enters the targeted cells via "receptor sites." Traditional counter-poisons and such (like Narcan for Morphine) work by blocking the receptor sites. As such, Narcan (which shares the same receptor sites as Morphine) blocks the Morphine receptor sites, preventing continued metabolization of morphine and its effects.
Scientists did some work on mice a while back by genetically removing morphine receptor sites, thus making Morphine have no effect on the mice and making them unable to become addicted to it. The mice would not push buttons to give them morphine, because having no effect on them, they never learned the behavior to associate the lever with the effects of morphine. Thus it was crudely called a "learning disability."
So if a substance has no effect on you at all, you never develop the learned behavior to associate pushing a lever to receive the substance (because you don't get a high or whatever from it).
The interesting thing to this though is that many chemicals and medicines are presumed to share receptor sites. Removal of receptor sites is fascinating but very preliminary because we still don't understand how they work or what chemicals share receptor sites with each other. By removing nicotine receptors are we also removing a receptor site for another, more important chemical?
-Kelly
Post a Comment