Nicotine-induced sensitization in mice: changes in locomotor activity and mesencephalic gene expression
Abstract
It is believed that drug-induced behavioral sensitization is an important process in the development of substance dependence. In order to explore mechanisms of sensitization, a mouse model of nicotine-induced locomotor sensitization was established, and effects of the sensitization process on mesencepahlic gene expression were examined. A schedule, which included 3 weeks of intermittent nicotine exposure (0.5 mg/kg, s.c.) and 3 weeks of withdrawal, resulted in locomotor sensitization. Effects of sensitization on mesencephalic expression of approximately 14,000 genes were assessed using oligonucleotide microarrays. Signal intensity differences in samples obtained from repeated nicotine- and saline-exposed animals were analyzed with z-test after False Discovery Rate (FDR) multiple test correction. Genes related to GABA-A receptors and protein phosphatases were among 68 genes showing significantly different expression levels between the saline and the nicotine groups. We hypothesize that some of the gene expression changes in the mesencephalon are involved in pathways leading to nicotine-induced sensitization. Down-regulation of GABA-A receptors induced by repeated nicotine exposure may facilitate dopaminergic neuronal transmission and may contribute to increased locomotor activity.
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Increases in VTA α1GABAAR expression parallel behavioral sensitization to the effects of nicotine and cocaine.
“On the contrary, chronic nicotine [118] or cocaine [119] increases VTA α1GABAAR expression, paralleling behavioral sensitization to the effects of these drugs.”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [118]
Chronic nicotine increases VTA α1GABAAR expression.
“On the contrary, chronic nicotine [118] or cocaine [119] increases VTA α1GABAAR expression, paralleling behavioral sensitization to the effects of these drugs.”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [118]
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- Authors
- Saito, M., O’Brien, D., Kovacs, K. M., Wang, R., Zavadil, J., & Vadasz, C.
- Affiliations
- Nathan Kline Institute for Psychiatric Research (US)
- Corresponding author
- Saito, Mariko
- ORCID
- Saito, Mariko
- Venue
- Neurochemical Research
- Published
- 2005-08
- Volume
- 30
- Issue
- 8
- Pages
- 1027-1035
- ISSN
- 0364-3190 (ISSN-L)
- 1573-6903
- OpenAlex
- W2013649622
- Cited by
- 14
- References
- 33
- Citations by year
- 2023: 1 · 2021: 1 · 2018: 1 · 2015: 1 · 2013: 2 · 2012: 1
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurochemical Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Philip Morris International
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- nicotine, locomotor sensitization, midbrain, gene expression, GABAA receptor, protein phosphatase, nicotine withdrawal, dopamine signaling, substance dependence, mouse model
- MeSH terms
- Animals, Base Sequence, Behavior, Animal, Female, Gene Expression Regulation, Mesencephalon, Mice, Inbred BALB C, Mice, Inbred C57BL, Molecular Sequence Data, Motor Activity, Nicotine, Mice
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