This Research was conducted to determine whether or not prenatal (prenatal being the time after conception but before birth; gestation) exposure to nicotine would alter nicotinic receptors in the brains of mice. This research was initiated because although there is conclusive evidence that maternal (referring to the pregnant mother) smoking during pregnancy may effect the development of a child, little is known about the mechanisms that are potentially responsible for these effects. As it is well known, maternal smoking may result in pregnancy complications, low birth weight, a higher prenatal mortality rate, and long term effects on the physical, emotional, and intellectual development of a child. Nicotine being the most potent psychoactive component of tobacco, it was the most suspected cause of these birth defects and physiological changes therefore sparking this research. Test Subjects In order for this research to be valid, a mammalian subject with brain responses relatively close to that of humans had to be chosen for the testing. Another aspect taken into consideration was obviously an ethics / moral issue: since the animals had to be sacrificed in order to conduct the research, they had to be dispensable and relatively meaningless.
(No cute and cuddly ones either! ) Selecting mice compromised this happy medium. Although the neurological workings are greatly different and much more simplex in a mouse than in a human, the basic responses would still be intact therefore the research would give sufficient usable data that could be used for beneficial study. Not to mention, mice arent that cute and are pretty plentiful in the grand scheme of the Eco-system. (That should keep Meryl l Streep and Jane Fonda in line) Testing Materials The Chemicals used in this study were a chemical form of nicotine, a similar chemical that deals wit the same receptors as nicotine, and a straight saline solution. These three solutions were tested in three separate groups: nicotine infused, a saline infused, and a control. The Test After the mice were mated and conception was guaranteed (the formation of vaginal plugs detected), the mothers were separated into three separate groups.
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Approximately 1 day after conception, the three testing agents (chemicals) began to be administered to the three test groups. Upon parturition (giving birth), the mothers immediately stopped receiving the chemicals and they and their litters were secluded into their own cages apart from the other litters. The offspring were then sacrificed periodically on postnatal days (after birth) to insure the detection of nicotine receptor changes in conjunction with development. The daily intervals went 0, 5, 10, 20, 30, and 60 days. Upon being sacrificed (by means of cervical dislocation), the brains were removed, rinsed with distilled water, and dissected into seven brain regions.
All of these regions were then put through a scientific process (which is very difficult to understand and nearly impossible to explain) to rid them from all remaining chemicals. After this process was completed, the brain regions were then tested against the chemical agents specific to their experimental groups to see how their response had be effected in contrast to one another. The Results Once the data was collected from each group there were some prominent differences and changes in the nicotinic receptors evident amongst the three groups. The group that received the nicotine chemical had a significantly higher response in the nicotine receptors of several of the brain regions than the other two groups. As the developmental intervals increased between parturition and sacrifice, the responses weakened indicating the breaking down of receptors and ultimately brain function which could be linked to birth defects and many other problems which have been associated with tobacco use of pregnant mothers. The second group which received a response provoking chemical much like nicotine also shared increases in receptor response and eventual weakening but not to the extent of nicotine.
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These also dulled brain function over time but at a small fraction of the result of nicotine binding. The third group, which received the saline infused solution, had little loss of receptor response and development is assumed to be at a normal rate and quality. Conclusion and Summation of Test Results Although these tests do not go to the extent of explaining how the use of tobacco (nicotine in general) causes birth defects, low birth weight, and other disorders, it does provide data which strongly suggests that prenatal exposure to nicotine can and does reduce function of neurological receptors that are key in development and all physiological activities. Though these tests may be considered by some to be irrelevant in relation with human response because of the distant physiological link of mice and man, even Big Tobacco cant ignore the fact that this is a definite milestone in the persistent trek to connect prenatal nicotine exposure to postnatal complications and developmental handicaps..