Cellular and Molecular Neurobiology

, Volume 8, Issue 3, pp 285–291

Hypothesis: A nicotine-dopamine interaction linking smoking with Parkinson's disease and tardive dyskinesia

  • Darrell G. Kirch
  • Anna -Maria Alho
  • Richard Jed Wyatt
Commentary

Summary

  1. 1.

    Nicotine, an important pharmacological component of cigarette smoke, is known to have significant effects on central nervous system (CNS) dopaminergic function. Although acute doses of nicotine have been shown to facilitate dopamine release, recent data indicate that chronic nicotine treatment may actually decrease CNS dopamine turnover in the striatum.

     
  2. 2.

    A number of epidemiological investigations have demonstrated that individuals who are or who have been smokers areless likely to develop idiopathic Parkinson's disease (a disorder involving a deficit in nigrostriatal dopaminergic neurotransmission). In addition, there is preliminary evidence that individuals with tardive dyskinesia (a hyperkinetic movement disorder observed in some cases of chronic neuroleptic treatment and thought by some to be associated with striatal dopamine receptor supersensitivity) aremore likely to be smokers.

     
  3. 3.

    A unitary hypothesis is presented, proposing that smoking in early adult life may decrease CNS catecholamine turnover, thereby protecting against free radical formation from catecholamine oxidation that in turn damages striatal neurons. These individuals are thereby “protected” from the later development of Parkinson's disease. In this hypothetical scheme, individuals who are given neuroleptics and who also are smokers may develop a greater degree of dopamine receptor supersensitivity due to combined receptor blockade by neuroleptics and a decrease in CNS dopamine turnover caused by nicotine, resulting in an increased prevalence of tardive dyskinesia in this group.

     

Key words

nicotine dopamine smoking Parkinson's disease tardive dyskinesia 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Arqueros, L., Naquira, D., and Zunino, E. (1978). Nicotine-induced release of catecholamines from rat hippocampus and striatum.Biochem. Pharmacol. 272667–2674.Google Scholar
  2. Balfour, D. J. K. (1982). The effects of nicotine on brain neurotransmitter systems.Pharmacol. Ther. 16269–282.Google Scholar
  3. Barochovsky, O., and Bradford, H. F. (1987). Modulation of dopamine release from neuron-enriched tissue cultures by cholinergic agents.J. Neurochem. 48798–803.Google Scholar
  4. Baron, J. A. (1986). Cigarette smoking and Parkinson's disease.Neurology 361490–1496.Google Scholar
  5. Benowitz, N. L. (1986). Clinical pharmacology of nicotine.Annu. Rev. Med. 37 21–32.Google Scholar
  6. Bharucha, N. E., Stokes, L., Schoenberg, B. S., Ward, C., Ince, S., Nutt, J. G., Eldridge, R., Calne, D. B., Mantel, N., and Duvoisin, R. (1986). A case-control study of twin pairs discordant for Parkinson's disease: A search for environmental risk factors.Neurology 36284–288.Google Scholar
  7. Binder, R. L., Kazamatsuri, H., Nishimura, T., and McNeil, D. E. (1987). Smoking and tardive dyskinesia.Biol. Psychiat. 22 1280–1282.Google Scholar
  8. Calne, D. B., and Langston, J. W. (1983). Aetiology of Parkinson's disease.Lancet 21457–1459.Google Scholar
  9. Clarke, P. B. S. (1987). Nicotine and smoking: A perspective from animal studies.Psychopharmacology 92135–143.Google Scholar
  10. Clarke, P. B. S., and Pert, A. (1985). Autoradiographic evidence for nicotine receptors on nigrostriatal and mesolimbic dopaminergic neurons.Brain Res. 348355–358.Google Scholar
  11. Clarke, P. B. S., Hommer, D. W., Pert, A., and Skirboll, L. R. (1985). Electrophysiological actions of nicotine on substantia nigra single units.Br. J. Pharmacol. 85 827–835.Google Scholar
  12. Cohen, G. (1984). Oxy-radical toxicity in catecholamine neurons.Neurotoxicology 577–82.Google Scholar
  13. Connelly, M. S., and Littleton, J. M. (1983). Lack of stereoselectivity in ability of nicotine to release dopamine from rat synaptosomal preparations.J. Neurochem. 411297–1302.Google Scholar
  14. Doll, R., and Peto, R. (1976). Mortality in relation to smoking: 20 years' observations on male British doctors.Br. Med. J. 21525–1536.Google Scholar
  15. Giorguieff-Chesselet, M. F., Kemel, M. L., Wandscheer, D., and Glowinski, J. (1979). Regulation of dopamine release by presynaptic nicotinic receptors in rat striatal slices: Effect of nicotine in a low concentration.Life Sci. 251257–1262.Google Scholar
  16. Godwin-Austen, R. B., Lee, P. N., Marmot, M. G., and Stern, G. M. (1982). Smoking and Parkinson's disease.J. Neurol. Neurosurg. Psychiat. 45577–581.Google Scholar
  17. Golbe, L. I., Cody, R. A., and Duvoisin, R. C. (1986). Smoking and Parkinson's disease: Search for a dose-response relationship.Arch. Neurol. 43774–778.Google Scholar
  18. Goodman, F. R. (1974). Effects of nicotine on distribution and release of14C-norepinephrine and14C-dopamine in rat brain striatum and hypothalamus slices.Neuropharmacology 131025–1032.Google Scholar
  19. Graham, D. G., Tiffany, S. M., Bell, W. R., and Gutknecht, W. F. (1978). Autoxidation versus covalent binding of quinones as the mechanism of toxicity of dopamine, 6-hydroxydopamine, and related compounds toward C1300 neuroblastoma cellsin vitro.Mol. Pharmacol. 14644–653.Google Scholar
  20. Jann, M. W., Saklad, S. R., Ereshefsky, L., Richards, A. L., Harrington, C. A., and Davis, C. M. (1986). Effects of smoking on haloperidol and reduced haloperidol plasma concentrations and haloperidol clearance.Psychopharmacology 90468–470.Google Scholar
  21. Jeste, D. V., and Wyatt, R. J. (1981). Dogma disputed: Is tardive dyskinesia due to postsynaptic dopamine receptor supersensitivty?J. Clin. Psychiat. 42455–457.Google Scholar
  22. Jeste, D. V., and Wyatt, R. J. (1982).Understanding and Treating Tardive Dyskinesia, Guilford Press, New York.Google Scholar
  23. Kahn, H. A. (1966). The Dorn study of smoking and mortality among U.S. veterans: Report on eight and one-half years of observation. InEpidemiological Approaches to the Study of Cancer and Other Chronic Diseases (W. Haenszel, Ed.), U.S. Department of Health, Education and Welfare, National Cancer Institute Monograph 19, pp. 1–27.Google Scholar
  24. Kirch, D. G., Gerhardt, G. A., Shelton, R. C., Freedman, R., and Wyatt, R. J. (1987). Effect of chronic nicotine administration on monoamine and monoamine metabolite concentrations in rat brain.Clin. Neuropharmacol. 10376–383.Google Scholar
  25. Langston, J. W. (1985). MPTP and Parkinson's disease.TINS 879–83.Google Scholar
  26. Lichtensteiger, W., Hefti, F., Felix, D., Huwyler, T., Melamed, E., and Schlumpf, M. (1982). Stimulation of nigrostriatal dopamine neurones by nicotine.Neuropharmacology 21963–968.Google Scholar
  27. Perry, T. L., Godin, D. V., and Hansen, S. (1982). Parkinson's disease: A disorder due to nigral glutathione deficiency?Neurosci. Lett. 33305–310.Google Scholar
  28. Pomerleau, O. F., and Pomerleau, C. S. (1984). Neuroregulators and the reinforcement of smoking: Towards a biobehavioral explanation.Neurosci. Biobehav. Rev. 8503–513.Google Scholar
  29. Rajput, A. H., Offord, K. P., Beard, C. M., and Kurland, L. T. (1987). A case-control study of smoking habits, dementia, and other illnesses in idiopathic Parkinson's disease.Neurology 37226–232.Google Scholar
  30. Todes, C. J., and Lees, A. J. (1985). The pre-morbid personality of patients with Parkinson's disease.J. Neurol. Neurosurg. Psychiat. 4897–100.Google Scholar
  31. Ward, C. D., Duvoisin, R. C., Ince, S. E., Nutt, J. D., Eldridge, R., and Calne, D. B. (1983). Parkinson's disease in 65 pairs of twins and in a set of quadruplets.Neurology 33815–824.Google Scholar
  32. Yassa, R., Lal, S., Korpassy, A., and Ally, J. (1987). Nicotine exposure and tardive dyskinesia.Biol. Psychiat. 2267–72.Google Scholar

Copyright information

© Plenum Publishing Corporation 1988

Authors and Affiliations

  • Darrell G. Kirch
    • 1
  • Anna -Maria Alho
    • 1
  • Richard Jed Wyatt
    • 1
  1. 1.Neuropsychiatry BranchNational Institute of Mental Health, William A. White BuildingWashington D.C.USA

Personalised recommendations