Nicotinic mechanisms influencing synaptic plasticity in the hippocampus
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Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the hippocampus, and nicotinic signaling plays an important role in neuronal function. In the context of learning and memory related behaviors associated with hippocampal function, a potentially significant feature of nAChR activity is the impact it has on synaptic plasticity. Synaptic plasticity in hippocampal neurons has long been considered a contributing cellular mechanism of learning and memory. These same kinds of cellular mechanisms are a factor in the development of nicotine addiction. Nicotinic signaling has been demonstrated by in vitro studies to affect synaptic plasticity in hippocampal neurons via multiple steps, and the signaling has also been shown to evoke synaptic plasticity in vivo. This review focuses on the nAChRs subtypes that contribute to hippocampal synaptic plasticity at the cellular and circuit level. It also considers nicotinic influences over long-term changes in the hippocampus that may contribute to addiction.
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Repeated nicotine exposure produces heterologous adaptations, including increased AMPA/NMDA current ratios at DA neurons and increased high-affinity D2 receptors in the NAcc.
“Besides altering cholinergic function, repeated nicotine exposure produces heterologous adaptations. For example, nicotine increases AMPA/NMDA current ratios (a hallmark of long-term potentiation) at DA neurons [94–96] and other locations involved in drug-associated memory [97–99]. In the NAcc, nicotine leads to an increase in high affinity DA D2 receptors [100].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [95]
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- Authors
- Placzek, A. N., Zhang, T. A., & Dani, J. A.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Dani, John Anthony
- ORCID
- Dani, John Anthony
- Venue
- Acta Pharmacologica Sinica
- Published
- 2009-05-11
- Volume
- 30
- Issue
- 6
- Pages
- 752-760
- ISSN
- 0253-9756 (ISSN-L)
- 1671-4083
- 1745-7254
- PMC
- PMC2864771
- OpenAlex
- W2055471148
- Cited by
- 77
- References
- 91
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 5 · 2020: 3 · 2019: 1 · 2018: 8 · 2017: 3 · 2016: 5 · 2015: 3 · 2014: 9 · 2013: 10 · 2012: 6
- FWCI
- 0.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Pharmacologica Sinica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (NS21229)
- National Institute on Drug Abuse (DA09411, R01DA009411)
- National Institute of Neurological Disorders and Stroke (NS 21229, R37NS021229, R01NS021229)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- nicotinic acetylcholine receptors, synaptic plasticity, hippocampus, learning and memory, nicotine dependence, nAChR subtypes, hippocampal circuitry
- MeSH terms
- Animals, Hippocampus, Humans, Synaptic Transmission, Neuronal Plasticity, Nicotine, Receptors, Nicotinic, Tobacco Use Disorder, Signal Transduction, Nicotinic Agonists, Protein Subunits
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