In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice
Open accessAbstract
The extracellular regulated kinase (ERK) pathway was studied to determine its role in neuronal plasticity related to the development of nicotine dependence. Levels and phosphorylation state of ERK, cAMP response element binding protein (CREB) and proline‐rich/Ca 2+‐activated tyrosine kinase (PYK2), and levels of tyrosine hydroxylase (TH), were determined using western blotting. C57Bl/6J mice received acute or chronic nicotine (200 µg/mL) in their drinking water or were withdrawn from nicotine for 24 h following chronic exposure. CREB phosphorylation was reduced in the nucleus accumbens following chronic nicotine, consistent with previous reports that decreased accumbens CREB activity increases drug reinforcement. In contrast, CREB phosphorylation was increased in the prefrontal cortex following chronic nicotine exposure and in the ventral tegmental area during nicotine withdrawal. In addition, total and phosphorylated ERK decreased in the amygdala following chronic nicotine exposure, but ERK phosphorylation increased in the prefrontal cortex. TH levels increased in both the amygdala and prefrontal cortex, supporting the hypothesis that increased catecholaminergic tone contributes to nicotine reinforcement. Overall, these results support a role for ERK and CREB activity in neural plasticity associated with nicotine dependence.
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In PFC, phosphorylation of ERK and CREB increases after repeated nicotine exposure.
“Specifically in the PFC, increases in phosphorylation of both these enzymes were found after repeated nicotine exposure (Brunzell et al. 2003).”
From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Brunzell et al. 2003
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References 85 · Cited by 176
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- Authors
- Brunzell, D. H., Russell, D. S., & Picciotto, M. R.
- Affiliations
- Yale University (US)
- Corresponding author
- Picciotto, Marina R.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2003-02-28
- Volume
- 84
- Issue
- 6
- Pages
- 1431-1441
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2073236029
- Cited by
- 176
- References
- 85
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 6 · 2020: 6 · 2019: 6 · 2018: 4 · 2017: 6 · 2016: 1 · 2015: 7 · 2014: 6 · 2013: 10 · 2012: 15
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Yale University
- National Institutes of Health (DA14241, DA00436)
- National Institute on Drug Abuse (DA14241, DA 13334, DA 00436, P50DA013334)
- 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 dependence, nicotine, ERK signaling, CREB phosphorylation, mesocorticolimbic system, nucleus accumbens, prefrontal cortex, ventral tegmental area, amygdala, nicotine withdrawal, tyrosine hydroxylase, neuroplasticity, drug reinforcement, chronic nicotine exposure
- MeSH terms
- Administration, Oral, Amygdala, Animals, Cotinine, Drug Administration Schedule, Limbic System, Male, Mesencephalon, Mice, Inbred C57BL, Nicotine, Nucleus Accumbens, Phosphorylation, Tobacco Use Disorder, Signal Transduction, Cyclic AMP Response Element-Binding Protein, Prefrontal Cortex, Ventral Tegmental Area, Nicotinic Agonists, Mitogen-Activated Protein Kinases, Mice
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