Cited by 181Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchSmoking Behavior and Cessation

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Regulation of synaptic transmission and plasticity by neuronal nicotinic acetylcholine receptors

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McKay, Bruce E., Placzek, Andon N., Dani, John A.·2007·Biochemical Pharmacology

DOI 10.1016/j.bcp.2007.07.001PMC PMC2047292

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Abstract

Nicotinic acetylcholine receptors (nAChRs) are widely expressed throughout the central nervous system and participate in a variety of physiological functions. Recent advances have revealed roles of nAChRs in the regulation of synaptic transmission and synaptic plasticity, particularly in the hippocampus and midbrain dopamine centers. In general, activation of nAChRs causes membrane depolarization and directly and indirectly increases the intracellular calcium concentration. Thus, when nAChRs are expressed on presynaptic membranes their activation generally increases the probability of neurotransmitter release. When expressed on postsynaptic membranes, nAChR-initiated calcium signals and depolarization activate intracellular signaling mechanisms and gene transcription. Together, the presynaptic and postsynaptic effects of nAChRs generate and facilitate the induction of long-term changes in synaptic transmission. The direction of hippocampal nAChR-mediated synaptic plasticity - either potentiation or depression - depends on the timing of nAChR activation relative to coincident presynaptic and postsynaptic electrical activity, and also depends on the location of cholinergic stimulation within the local network. Therapeutic activation of nAChRs may prove efficacious in the treatment of neuropathologies where synaptic transmission is compromised, as in Alzheimer's or Parkinson's disease.

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Authors: McKay, B. E., Placzek, A. N., & Dani, J. A.
Affiliations: Baylor College of Medicine (US)
Corresponding author: Dani, John A.
ORCID: Dani, John A.
Venue: Biochemical Pharmacology
Publisher: Elsevier BV
Published: 2007-10
Volume: 74
Issue: 8
Pages: 1120-1133
ISSN: 0006-2952 (ISSN-L)
DOI: 10.1016/j.bcp.2007.07.001
PMC: PMC2047292
OpenAlex: W1964188222
Cited by: 181
References: 181
Citations by year: 2026: 8 · 2025: 9 · 2024: 9 · 2023: 6 · 2022: 11 · 2021: 12 · 2020: 9 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 6 · 2015: 10 · 2014: 11 · 2013: 11 · 2012: 11
FWCI: 5.38
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochemical Pharmacology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
Natural Sciences and Engineering Research Council of Canada
National Institute on Drug Abuse
National Institute of Neurological Disorders and Stroke (T32NS043124, 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
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
Keywords: nicotinic acetylcholine receptors, synaptic transmission, synaptic plasticity, hippocampus, midbrain dopamine, presynaptic neurotransmitter release, intracellular signaling, long-term potentiation, long-term depression, cholinergic modulation, Alzheimer's disease, Parkinson's disease
MeSH terms: Animals, Hippocampus, Humans, Synaptic Transmission, Neuronal Plasticity, Receptors, Nicotinic, Signal Transduction, Ventral Tegmental Area, Long-Term Potentiation

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Regulation of synaptic transmission and plasticity by neuronal nicotinic acetylcholine receptors

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