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Research ArticleArticle

Increased Nicotinic Receptors in Brains from Smokers: Membrane Binding and Autoradiography Studies

David C. Perry, Martha I. Dávila-Garcı́a, Craig A. Stockmeier and Kenneth J. Kellar
Journal of Pharmacology and Experimental Therapeutics June 1999, 289 (3) 1545-1552;
David C. Perry
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Martha I. Dávila-Garcı́a
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Craig A. Stockmeier
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Kenneth J. Kellar
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Abstract

Chronic administration of nicotine increases the density of neuronal cholinergic nicotinic receptors in cells and in rodent brain, and similar increases have been reported in brains from human smokers. To further examine this phenomenon, we measured nicotinic receptor binding sites in brain regions from matched populations of smokers and nonsmokers. We first measured binding of [3H](±)epibatidine ([3H]EB) and [3H]cytisine in homogenate preparations from samples of prefrontal and temporal cerebral cortex. Binding of each radioligand was significantly higher (250–300%) in both cortical regions from brains of smokers. Frozen sections from each of the cerebral cortical regions and the hippocampus were used for autoradiographic analysis of [3H]EB binding. In cerebral cortex, binding was most dense in layer VI in the prefrontal cortex and layers IV and VI in the temporal cortex. Densitometric analysis of [3H]EB binding sites revealed marked increases of 300 to 400% of control in all cortical regions examined from smokers’ brains. Binding in the hippocampal formation was heterogeneously distributed, with dense areas of binding sites seen in the parasubiculum, subiculum, and molecular layer of the dentate gyrus, and the lacunosum-moleculare layer of the CA1/2. Binding of [3H]EB was significantly higher in all six regions of the hippocampus examined from brains of smokers compared with nonsmokers. These increases ranged from 160% of control in parasubiculum to 290% in the molecular layer of the dentate gyrus. The increase in nicotinic receptors in the cerebral cortex and hippocampus of smokers may modify the central nervous system effects of nicotine and contribute to an altered response of smokers to nicotine.

Footnotes

  • Send reprint requests to: Kenneth J. Kellar, Ph.D., Department of Pharmacology, Georgetown University School of Medicine, 3900 Reservoir Rd. NW, Washington, DC 20007. E-mail:kellark{at}gunet.georgetown.edu

  • ↵1 This work was supported by National Institutes of Health Grants DA06486, MH45488, and NS34706. Portions of this work were presented at meetings of the Society for Neuroscience (1996) and of the Society for Research in Nicotine and Tobacco (1996).

  • Abbreviations:
    EB
    epibatidine
    [3H]EB
    [3H](±)epibatidine
    PMI
    postmortem interval
    • Received October 30, 1998.
    • Accepted February 4, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 289 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 289, Issue 3
1 Jun 1999
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Research ArticleArticle

Increased Nicotinic Receptors in Brains from Smokers: Membrane Binding and Autoradiography Studies

David C. Perry, Martha I. Dávila-Garcı́a, Craig A. Stockmeier and Kenneth J. Kellar
Journal of Pharmacology and Experimental Therapeutics June 1, 1999, 289 (3) 1545-1552;

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Research ArticleArticle

Increased Nicotinic Receptors in Brains from Smokers: Membrane Binding and Autoradiography Studies

David C. Perry, Martha I. Dávila-Garcı́a, Craig A. Stockmeier and Kenneth J. Kellar
Journal of Pharmacology and Experimental Therapeutics June 1, 1999, 289 (3) 1545-1552;
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