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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Tobacco smoking induces expression of very-high-affinity nicotine binding sites on blood polymorphonuclear cells.

The targets of nicotine in the central nervous system (CNS) have been identified as nicotinic acetylcholine (ACh) receptors. Because of their localization in the brain, no data are available about their in vivo modifications. However, nonneuronal nicotine binding sites have been identified on peripheral blood cells. The present study was designed to evaluate the effects of tobacco smoking on granulocyte nicotine binding sites. Binding assays were performed on granulocyte membranes using (-)(3H)nicotine and were analyzed by the Scatchard method in nonsmokers (n=10), smokers (n=10), and ex-smokers (n=10). In nonsmokers, a single-affinity binding site was detected with Kd = 1.08 +/- 0.05 x 10 -9 M. In contrast, in smokers, two different classes of binding sites were identified: one with Kd1 = 2.80 +/- 0.81 x 10 -11 M and another with Kd2 = 3.92 +/- 0.58 x 10 -9 M, similar to the binding site in nonsmokers. Moreover, a twofold increase in nicotine binding-site density was observed in smokers. Ex-smokers recovered a single class of binding sites similar to those observed in nonsmokers when they had stopped smoking for more than 1 yr, whereas recent ex-smokers (1 to 8 mo) displayed a pattern similar to that in smokers, as demonstrated by the persistence of two classes of nicotine binding sites. Chronic nicotine exposure induces modifications of nicotine binding sites on granulocytes. It is noteworthy that the persistence of such alterations corresponds to the very high rate of relapse into smoking observed during the early stages of tobacco cessation. Consequently, monitoring of nicotine binding sites could constitute an interesting approach to understanding the pharmacologic mechanisms involved in tobacco dependence.[1]

References

  1. Tobacco smoking induces expression of very-high-affinity nicotine binding sites on blood polymorphonuclear cells. Lebargy, F., Benhammou, K., Morin, D., Zini, R., Urien, S., Brée, F., Bignon, J., Branellec, A., Lagrue, G. Am. J. Respir. Crit. Care Med. (1996) [Pubmed]
 
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