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Cited by 67Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchSmoking Behavior and Cessation

A Non-α7 Nicotinic Acetylcholine Receptor Modulates Excitatory Input to Hippocampal CA1 Interneurons

Alkondon, Manickavasagom, Albuquerque, Edson X.·2002·Journal of Neurophysiology
DOI 10.1152/jn.00708.2001
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Abstract

The nicotinic acetylcholine receptor (nAChR), particularly the α7 subtype, has received profound attention for its role in modifying excitatory postsynaptic currents (EPSCs) in hippocampal pyramidal neurons as well as in neurons from other brain regions. Here, we tested the possibility that an nAChR could affect EPSCs in the interneurons of rat hippocampal slices. Using whole-cell patch-clamp technique on CA1 stratum radiatum interneurons and U-tube application of agents, we show that nicotinic agonists enhance EPSC frequency in interneurons. Among the agents tested, cytisine and mecamylamine were the most effective agonist and antagonist, respectively, suggesting a role for α3β4-containing nAChRs in the modulation of interneuron EPSCs. Ligands selective for the α7 nAChR had very little or no effect on interneuron EPSCs. Low concentrations of nicotine also enhanced EPSC frequency, implicating the involvement of non-α7 nAChRs in controlling interneuron excitability in smokers. We conclude that nAChR-dependent EPSC modulation in the hippocampus is both subtype- and neuron-specific and that a non-α7 nAChR, presumably α3β4, controls glutamate transmission to CA1 interneurons.

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  • Nicotinic receptor activation enhances the influence of afferent synaptic input in the hippocampus, including glutamatergic input to interneurons.

    “Similar to thalamic input to neocortex, nicotinic receptor activation enhances the influence of afferent synaptic input in the hippocampus (Radcliffe and Dani, 1998; Giocomo and Hasselmo, 2005) including glutamatergic input to interneurons (Alkondon and Albuquerque, 2002).”

    From Modes and models of forebrain cholinergic neuromodulation of cognition (2011) · cites this paper as Alkondon and Albuquerque, 2002

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Authors
Alkondon, M., & Albuquerque, E. X.
Affiliations
  • University of Maryland, Baltimore (US)
  • Universidade Federal do Rio de Janeiro (BR)
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
2002-03-01
Volume
87
Issue
3
Pages
1651-1654
ISSN
  • 0022-3077 (ISSN-L)
  • 1522-1598
DOI
10.1152/jn.00708.2001
OpenAlex
W2308629448
Cited by
67
References
18
Citations by year
2025: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2017: 1 · 2015: 2 · 2014: 3 · 2013: 3 · 2012: 1
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurophysiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01es005730-07)
  • National Institute of Neurological Disorders and Stroke (R01NS025296, R01NS041671, NS 25296, NS 41671)
  • National Institute of Environmental Health Sciences (ES 05730)
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
nicotinic acetylcholine receptors, α3β4 nAChR, excitatory postsynaptic currents, glutamatergic neurotransmission, nicotine, cytisine, mecamylamine, interneuron excitability, cholinergic modulation
MeSH terms
Quinolizidine Alkaloids, Acetylcholine, Alkaloids, Animals, Azocines, Choline, Dihydro-beta-Erythroidine, Dimethylphenylpiperazinium Iodide, Hippocampus, Interneurons, Mecamylamine, Nicotine, Quinolizines, Receptors, Nicotinic, Rats, Sprague-Dawley, Patch-Clamp Techniques, Nicotinic Agonists, Nicotinic Antagonists, Excitatory Postsynaptic Potentials, Rats, alpha7 Nicotinic Acetylcholine Receptor

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