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Cited by 135Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationParkinson's Disease Mechanisms and Treatments

Dopamine and nicotinic receptor binding and the levels of dopamine and homovanillic acid in human brain related to tobacco use

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Court, J.A, Lloyd, S, Thomas, N, Piggott, M.A, Marshall, E.F, Morris, C.M, Lamb, H, Perry, R.H +2 more·1998·Neuroscience
DOI 10.1016/s0306-4522(98)00088-8
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Abstract

Reports of a reduction in the risk of developing Parkinson's disease and Alzheimer's disease in tobacco smokers, together with the loss of high-affinity nicotine binding in these diseases, suggest that consequences of nicotinic cholinergic transmission may be neuroprotective. Changes in brain dopaminergic parameters and nicotinic receptors in response to tobacco smoking have been assessed in this study of autopsy samples from normal elderly individuals with known smoking histories and apolipoprotein E genotype. The ratio of homovanillic acid to dopamine, an index of dopamine turnover, was reduced in elderly smokers compared with age matched non-smokers (P<0.05) in both the caudate and putamen. Dopamine levels were significantly elevated in the caudate of smokers compared with non-smokers (P<0.05). However there was no significant change in the numbers of dopamine (D1, D2 and D3) receptors or the dopamine transporter in the striatum, or for dopamine D1 and D2 receptors in the hippocampus in smokers compared with non-smokers or ex-smokers. The density of high-affinity nicotine binding was higher in smokers than non-smokers in the hippocampus, entorhinal cortex and cerebellum (elevated by 51-221%) and to a lesser extent in the striatum (25-55%). The density of high-affinity nicotine binding in ex-smokers was similar to that of the non-smokers in all the areas investigated. The differences in high-affinity nicotine binding between smokers and the non- and ex-smokers could not be explained by variation in apolipoprotein E genotype. There were no differences in alpha-bungarotoxin binding, measured in hippocampus and cerebellum, between any of the groups. These findings suggest that chronic cigarette smoking is associated with a reduction of the firing of nigrostriatal dopaminergic neurons in the absence of changes in the numbers of dopamine receptors and the dopamine transporter. Reduced dopamine turnover associated with increased numbers of high-affinity nicotine receptors is consistent with attenuated efficacy of these receptors in smokers. A decrease in striatal dopamine turnover may be a mechanism of neuroprotection in tobacco smokers that could delay basal ganglia pathology. The current findings are also important in the interpretation of measurements of nicotinic receptors and dopaminergic parameters in psychiatric conditions such as schizophrenia, in which there is a high prevalence of cigarette smoking.

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  • Nicotine-induced up-regulation of nAChRs has been replicated in systems ranging from clonal cell lines to primary neurons in culture, mouse models, and smokers' brains.

    “Nicotine-induced “up-regulation” has been replicated many times in systems ranging from clonal cell lines to primary neurons in culture, to mouse models, and to smokers’ brains (Breese et al., 1997; Court et al., 1998; Staley et al., 2006; Mukhin et al., 2008; Albuquerque et al., 2009; Lester et al., 2009).”

    From Nicotine up-regulates α4β2 nicotinic receptors and ER exit sites via stoichiometry-dependent chaperoning (2011) · cites this paper as Court et al., 1998

  • Postmortem tissue studies observed receptor densities in exsmokers similar to those in nonsmokers after more than 2 months of smoking cessation.

    “Receptor densities in exsmokers that were similar to those in nonsmokers after more than 2 mo of smoking cessation were observed previously in postmortem tissue (5,6).”

    From Greater Nicotinic Acetylcholine Receptor Density in Smokers Than in Nonsmokers: A PET Study with 2-<sup>18</sup>F-FA-85380 (2008) · cites this paper as [6]

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Authors
Court, J. A., Lloyd, S., Thomas, N., Piggott, M. A., Marshall, E. F., Morris, C. M., Lamb, H., Perry, R. H., Johnson, M., & Perry, E. K.
Affiliations
Newcastle University (GB)
Corresponding author
Court, J.A
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
1998-06
Volume
87
Issue
1
Pages
63-78
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/s0306-4522(98)00088-8
OpenAlex
W2077730162
Cited by
135
References
130
Citations by year
2026: 1 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 5 · 2013: 4 · 2012: 4
FWCI
3.77
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Newcastle University ePrints (Newcastle Univesity)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
smoking, nicotinic acetylcholine receptors, dopamine turnover, homovanillic acid, dopamine receptors, dopamine transporter, APOE genotype, former smokers, nigrostriatal dopaminergic neurons, striatum, hippocampus, neuroprotection, Parkinson's disease, Alzheimer's disease, schizophrenia, alpha-bungarotoxin binding
MeSH terms
Age Factors, Aged, Aged, 80 and over, Apolipoproteins E, Brain, Bungarotoxins, Carrier Proteins, Cerebellum, Corpus Striatum, Dopamine, Female, Hippocampus, Homovanillic Acid, Humans, Male, Membrane Glycoproteins, Middle Aged, Nerve Tissue Proteins, Receptors, Dopamine, Receptors, Nicotinic, Sex Factors, Smoking, Receptors, Dopamine D1, Receptors, Dopamine D2, Membrane Transport Proteins, Dopamine Plasma Membrane Transport Proteins, Receptors, Dopamine D3

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