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Cited by 1,070Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchSmoking Behavior and Cessation

Nicotine enhancement of fast excitatory synaptic transmission in CNS by presynaptic receptors

McGehee, Daniel S., Heath, Mark J. S., Gelber, Shari, Devay, Piroska, Role, Lorna W.·1995·Science
DOI 10.1126/science.7569895
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Abstract

The behavioral and cognitive effects of nicotine suggest that nicotinic acetylcholine receptors (nAChRs) participate in central nervous system (CNS) function. Although nAChR subunit messenger RNA (mRNA) and nicotine binding sites are common in the brain, there is little evidence for synapses mediated by nAChRs in the CNS. To test whether, CNS nAChRs might modify rather than mediate transmission, the regulation of excitatory synaptic transmission by these receptors was examined. Nanomolar concentrations of nicotine enhanced both glutamatergic and cholinergic synaptic transmission by activation of presynaptic nAChRs that increased presynaptic [Ca2]i. Pharmacological and subunit deletion experiments reveal that these presynaptic nAChRs include the alpha 7 subunit. These findings reveal that CNS nAChRs enhance fast excitatory transmission, providing a likely mechanism for the complex behavioral effects of nicotine.

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Crossref · 10.1126/science.7569895

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  • Nicotine has a cascading effect on central neurotransmission resulting in the release of norepinephrine, histamine, GABA and glutamate.

    “In addition, nicotine has a cascading effect on central neurotransmission also resulting in the release of norepinephrine and histamine as well as GABA and glutamate (28, 29).”

    From The detrimental effects of smoking on the course and outcome in adults with bipolar disorder—A narrative review (2023) · cites this paper as [28]

  • Nicotinic acetylcholine receptors are not clustered at postsynaptic membranes apposed to sites of acetylcholine release, but are rather dispersed along the surface and intracellular compartments of neurons, including presynaptic terminals, cell bodies and axons.

    “nAChRs are not clustered at postsynaptic membranes apposed to sites of ACh release, but are rather dispersed along the surface (and intracellular compartments) of neurons, including presynaptic terminals (McGehee et al., 1995; Vidal and Changeux, 1993), cell bodies and even axons (Arroyo-Jimenez et al., 1999; Hill Jr. et al., 1993; Kawai et al., 2007).”

    From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as McGehee et al., 1995

  • Stimulation of nicotinic acetylcholine receptors can increase the release of glutamate, GABA, dopamine, acetylcholine, norepinephrine, and serotonin.

    “In addition, stimulation of nAChRs can increase the release of glutamate, GABA, dopamine (DA), ACh, norepinephrine, and serotonin (McGehee et al., 1995; Wonnacott, 1997) (Figure 1).”

    From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as McGehee et al., 1995

  • Acetylcholine released in the VTA is likely to potentiate glutamatergic synaptic transmission onto dopamine neurons through α7 nicotinic receptors, and may therefore increase the likelihood of burst firing of these neurons.

    “ACh released in the VTA is likely to potentiate glutamatergic synaptic transmission onto DA neurons through α7 nAChRs, and may therefore increase the likelihood of burst firing of these neurons (Grenhoff et al., 1986; Maskos, 2008; McGehee et al., 1995).”

    From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as McGehee et al., 1995

  • Glutamatergic transmission can be facilitated by the presynaptic action of nicotine.

    “Glutamatergic transmission can be facilitated by the presynaptic action of nicotine (McGehee et al., 1995), which then may activate dopaminergic neurons.”

    From Dopamine reward circuitry: Two projection systems from the ventral midbrain to the nucleus accumbens–olfactory tubercle complex (2007) · cites this paper as McGehee et al., 1995

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Authors
McGehee, D. S., Heath, M. J. S., Gelber, S., Devay, P., & Role, L. W.
Affiliations
  • Columbia University (US)
  • Department of Cell Biology and Anatomy in the Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1995-09-22
Volume
269
Issue
5231
Pages
1692-1696
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.7569895
OpenAlex
W2062419094
Cited by
1,070
References
46
Citations by year
2026: 3 · 2025: 14 · 2024: 11 · 2023: 10 · 2022: 11 · 2021: 22 · 2020: 20 · 2019: 9 · 2018: 19 · 2017: 18 · 2016: 17 · 2015: 28 · 2014: 30 · 2013: 34 · 2012: 29
FWCI
21.84
Type
journal article
Language
en
Open access
closed
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1f32ns009395-01)
  • National Institute of Neurological Disorders and Stroke (NS09395, NS22061, R01NS022061)
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 › Physiology › Smoking Behavior and Cessation
Keywords
nicotine, nicotinic acetylcholine receptors, presynaptic receptors, excitatory synaptic transmission, glutamatergic synapses, cholinergic synapses, presynaptic calcium, central nervous system
MeSH terms
Animals, Base Sequence, Binding Sites, Brain, Bungarotoxins, Calcium, Chick Embryo, Ganglia, Sympathetic, Molecular Sequence Data, Synaptic Transmission, Nicotine, Receptors, Nicotinic, Synapses, Thalamic Nuclei, Presynaptic Terminals, Glutamic Acid, Nicotinic Agonists, Culture Techniques

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