Nicotinic–serotonergic interactions in brain and behaviour
Abstract
This review focuses on nicotinic--serotonergic interactions in the central nervous system (CNS). Nicotine increases 5-hydroxytryptamine (5-HT) release in the cortex, striatum, hippocampus, dorsal raphé nucleus (DRN), hypothalamus, and spinal cord. As yet, there is little firm evidence for nicotinic receptors on serotonergic terminals and thus nicotine's effects on 5-HT may not necessarily be directly mediated, but there is strong evidence that the 5-HT tone plays a permissive role in nicotine's effects. The effects in the cortex, hippocampus, and DRN involve stimulation of 5-HT(1A) receptors, and in the striatum, 5-HT(3) receptors. The 5-HT(1A) receptors in the DRN play a role in mediating the anxiolytic effects of nicotine and the 5-HT(1A) receptors in the dorsal hippocampus and lateral septum mediate its anxiogenic effects. The increased startle and anxiety during nicotine withdrawal is mediated by 5-HT(1A) and 5-HT(3) receptors. The locomotor stimulant effect of acute nicotine is mediated by 5-HT(1A) receptors and 5-HT(2) receptors may play a role in the expression of a sensitised response after chronic nicotine treatment. Unfortunately, the role of 5-HT(1A) receptors in mediating nicotine seeking has not yet been investigated and would seem an important area for future research. There is also evidence for nicotinic--serotonergic interactions in the acquisition of the water maze, passive avoidance, and impulsivity in the five-choice serial reaction task.
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Nicotine, signaling through nAChRs, can influence serotonergic transmission in a complex manner, generally acting to increase serotonin release in many brain regions, including the hypothalamus.
“Nicotine, signaling through nAChRs, can influence serotonergic transmission in a complex manner, generally acting to increase serotonin release in many brain regions (reviewed in Seth et al., 2002), including the hypothalamus (Ramos et al., 2004).”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Seth et al., 2002
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- Authors
- Seth, P., Cheeta, S., Tucci, S., & File, S. E.
- Affiliations
- King's College London (GB)
- Corresponding author
- File, Sandra E.
- ORCID
- Cheeta, Survjit
- Venue
- Pharmacology Biochemistry and Behavior
- Publisher
- Elsevier BV
- Published
- 2002-04
- Volume
- 71
- Issue
- 4
- Pages
- 795-805
- ISSN
- 0091-3057 (ISSN-L)
- OpenAlex
- W2033178939
- Cited by
- 145
- References
- 124
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 6 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 8 · 2015: 3 · 2014: 7 · 2013: 8 · 2012: 5
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pharmacology Biochemistry and Behavior (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- nicotine, serotonin, 5-HT1A receptor, 5-HT3 receptor, 5-HT2 receptor, dorsal raphe nucleus, dorsal hippocampus, striatum, anxiolytic effects, anxiogenic effects, nicotine withdrawal, startle response, locomotor stimulant effects, sensitization, nicotine seeking, impulsivity, water maze, passive avoidance
- MeSH terms
- Central Nervous System Stimulants, Animals, Anxiety, Behavior, Behavior, Animal, Brain, Humans, Synaptic Transmission, Receptors, Nicotinic, Receptors, Serotonin, Reward
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