Chronic pre-treatment with nicotine enhances nicotine-evoked striatal dopamine release and α6 and β3 nicotinic acetylcholine receptor subunit mRNA in the substantia nigra pars compacta of the rat

Visanji, N.P.; Mitchell, S.N.; O'Neill, M.J.; Duty, S.

doi:10.1016/j.neuropharm.2005.07.013

Cited by 25Nicotinic Acetylcholine Receptors StudySmoking Behavior and CessationNeurotransmitter Receptor Influence on Behavior

Chronic pre-treatment with nicotine enhances nicotine-evoked striatal dopamine release and α6 and β3 nicotinic acetylcholine receptor subunit mRNA in the substantia nigra pars compacta of the rat

Visanji, N.P., Mitchell, S.N., O'Neill, M.J., Duty, S.·2006·Neuropharmacology

DOI 10.1016/j.neuropharm.2005.07.013

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Abstract

Whilst local intrastriatal infusion of nicotine consistently elicits striatal dopamine release, systemic administration often fails to do so. Since chronic nicotine administration is known to result in desensitisation-induced upregulation of nicotinic acetylcholine receptors (nAChRs), the present study investigated whether chronic pre-treatment could enhance the response to systemic nicotine and, if so, whether increases in specific nAChR subunit mRNA levels in the substantia nigra pars compacta (SNc) may underlie this effect. In vivo microdialysis studies in male Sprague-Dawley rats revealed that following 4 days pre-treatment with nicotine (0.8 mg kg(-1)s.c.), local intrastriatal nicotine infusion (3 mM) elicited significantly higher dopamine efflux compared to vehicle pre-treated controls (peak release: 1273 +/- 199% basal versus 731 +/- 113% basal), whereas systemic nicotine challenge (0.8 mg kg(-1)s.c.) elicited no response. In contrast, following 8 days pre-treatment with nicotine (0.8 mg kg(-1)s.c.), systemic nicotine challenge (0.8 mg kg(-1)s.c.) now produced significantly higher dopamine efflux than that of vehicle pre-treated controls (147 +/- 30% basal versus 91 +/- 5% basal). Eight days pre-treatment with nicotine also significantly elevated the levels of alpha6 (approximately 55%) and beta3 (approximately 43%) nAChR subunit mRNA in the SNc, suggesting that up-regulation of these nAChR subunit genes in the nigrostriatal tract may contribute to the enhanced nicotine-evoked striatal dopamine release.

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These effects on dopaminergic terminals extend and confirm other reports that chronic nicotine increases nicotine-induced dopamine release and upregulates receptors in striatum.
“These effects on dopaminergic terminals extend and confirm other reports that chronic nicotine increases nicotine-induced dopamine release (25,26) and upregulates receptors in striatum (5).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [26]

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Authors: Visanji, N. P., Mitchell, S. N., O'Neill, M. J., & Duty, S.
Affiliations: King's College London (GB)
Eli Lilly (United Kingdom) (GB)
Corresponding author: Duty, S.
ORCID: Visanji, N.P.
Duty, S.
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 2006-01
Volume: 50
Issue: 1
Pages: 36-46
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/j.neuropharm.2005.07.013
OpenAlex: W2113382092
Cited by: 25
References: 44
Citations by year: 2026: 1 · 2025: 1 · 2021: 1 · 2019: 1 · 2015: 1 · 2014: 2 · 2013: 4
FWCI: 0.75
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
Research Portal (King's College London) (submittedVersion)
Funders: Eli Lilly and Company
Medical Research Council
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 › Neurotransmitter Receptor Influence on Behavior
Keywords: nicotine, striatal dopamine release, nicotinic acetylcholine receptors, substantia nigra pars compacta, receptor up-regulation, desensitization, nigrostriatal pathway, dopamine efflux
MeSH terms: Animals, Autoradiography, Dopamine, Male, Nicotine, Receptors, Nicotinic, RNA, Messenger, Substantia Nigra, Sympathectomy, Chemical, Sympatholytics, Oxidopamine, Rats, Sprague-Dawley, In Situ Hybridization, Microdialysis, Nicotinic Agonists, Rats

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Chronic pre-treatment with nicotine enhances nicotine-evoked striatal dopamine release and α6 and β3 nicotinic acetylcholine receptor subunit mRNA in the substantia nigra pars compacta of the rat

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