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Cited by 67Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeuroscience and Neuropharmacology Research

Regulation of nicotinic receptors in the brain of mice withdrawn from chronic oral nicotine treatment

Pietilä, K., Lähde, Terhi, Attila, Martti, Ahtee, Liisa, Nordberg, Agneta·1998·Naunyn-Schmiedeberg's Archives of Pharmacology
DOI 10.1007/pl00005152
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Abstract

The effect of nicotine withdrawal on regional regulation of brain nicotinic receptors was studied in mice after chronic administration of nicotine in the drinking water for 2, 4 or 7 weeks. Two weeks of chronic nicotine administration did not alter the binding of [3H]-nicotine in the midbrain, cortex or cerebellum of the mice, while after both 4-and 7-week treatments a significant increase in the specific [3H]-nicotine binding was observed in cortical and midbrain membranes. In the midbrain, the [3H]-nicotine binding was increased by about 40% in mice withdrawn for 48-72 h from the 4-week chronic nicotine treatment and in mice withdrawn for 48 h from the 7-week treatment. The [3H]-nicotine binding was significantly increased (by 55-65%) in the cortex at 48 h and 72 h after withdrawal from 4-week chronic nicotine and it was even somewhat more increased (by 72-66%) after 7-week treatment. The cortical [3H]-nicotine binding was not altered at 24 h after the 4-week treatment, but in mice withdrawn for 24 h from the 7-week treatment it was increased by 116%. The increases in [3H]-nicotine binding returned to control levels within 1 week after withdrawal. None of the studied treatments affected the [3H]-nicotine binding in the cerebellum. Tolerance towards nicotine-induced locomotor depression was only found in mice withdrawn for 24 h from the 7-week chronic nicotine administration. These findings suggest that at least 4-week chronic nicotine administration in the drinking water is needed before any upregulation of nicotinic receptors can be observed. Furthermore, in our experiments the increase in the [3H]-nicotine binding was seen before behavioural tolerance could be demonstrated. The differences between brain regions in the time course of nicotinic receptor upregulation may reflect variations in nicotinic receptor subunits and their sensitivity to chronic nicotine treatment.

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  • Preclinical studies have demonstrated that nAChR levels return to control levels after termination of nicotine exposure, but with great variability in the time course.

    “Preclinical studies have demonstrated that nAChR levels return to control levels after termination of nicotine exposure, but with great variability in the time course15-17.”

    From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [15]

  • Previous preclinical studies demonstrated that in chronically nicotine treated animals, nAChR levels returned to levels observed in control animals after termination of nicotine, but with variable timing ranging between 1 and 3 weeks.

    “Previous preclinical studies demonstrated that in chronically nicotine treated animals, nAChR levels returned to levels observed in control animals after termination of nicotine, but with variable timing ranging between 1 and 3 weeks15, 80, 81.”

    From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [15]

  • Upregulation of nAChR expression can persist for several days after termination of chronic nicotine.

    “Additionally, studies have demonstrated that upregulation of nAChR expression can persist for several days following termination of chronic nicotine (Pietila et al. 1998; Staley et al. 2006).”

    From Nicotine Withdrawal (2015) · cites this paper as Pietila et al. 1998

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Related

Authors
Pietilä, K., Lähde, T., Attila, M., Ahtee, L., & Nordberg, A.
Affiliations
  • University of Helsinki (FI)
  • Karolinska Institutet (SE)
ORCID
Nordberg, Agneta
Venue
Naunyn-Schmiedeberg's Archives of Pharmacology
Publisher
Springer Science and Business Media LLC
Published
1998-01-28
Volume
357
Issue
2
Pages
176-182
ISSN
0028-1298 (ISSN-L)
DOI
10.1007/pl00005152
OpenAlex
W2072854024
Cited by
67
References
33
Citations by year
2021: 1 · 2019: 2 · 2018: 2 · 2016: 1 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 3
FWCI
1.16
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Naunyn-Schmiedeberg s Archives of Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Academy of Finland
  • Suomen Kulttuurirahasto
  • Vetenskapsrådet
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
nicotinic acetylcholine receptors, nicotine withdrawal, chronic nicotine administration, receptor up-regulation, midbrain, cerebral cortex, cerebellum, locomotor depression, tolerance (pharmacology and immunology)
MeSH terms
Administration, Oral, Animals, Brain Chemistry, Cerebellum, Cerebral Cortex, Mesencephalon, Motor Activity, Nicotine, Receptors, Nicotinic, Substance Withdrawal Syndrome, Up-Regulation, Nicotinic Agonists, Mice

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