Cited by 52Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Nicotinic modulation of glutamatergic synaptic transmission in region CA3 of the hippocampus

Giocomo, Lisa M., Hasselmo, Michael E.·2005·European Journal of Neuroscience

Abstract

Cholinergic modulation of synaptic transmission in the hippocampus appears to be involved in learning, memory and attentional processes. In brain slice preparations of hippocampal region CA3, we have explored the effect of nicotine on the afferent connections of stratum lacunosum moleculare (SLM) vs. the intrinsic connections of stratum radiatum (SR). Nicotine application had a lamina‐selective effect, causing changes in synaptic transmission only in SLM. The nicotinic effect in SLM was characterized by a transient decrease in synaptic potential size followed by a longer period of enhancement of synaptic transmission. The effect was blocked by γ‐aminobutyric acid (GABA)ergic antagonists, indicating the role of GABAergic interneurons in the observed nicotinic effect. The biphasic nature of the nicotinic effect could be due to a difference in receptor subtypes, as supported by the effects of the nicotinic antagonists mecamylamine and methyllycaconitine. Nicotinic modulation of glutamatergic synaptic transmission could complement muscarinic suppression of intrinsic connections, amplifying incoming information and providing a physiological mechanism for the memory‐enhancing effect of nicotine.

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Crossref · 10.1111/j.1460-9568.2005.04316.x

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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 Giocomo and Hasselmo, 2005

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Authors
Giocomo, L. M., & Hasselmo, M. E.
Affiliations
Boston University (US)
Venue
European Journal of Neuroscience
Publisher
Wiley
Published
2005-09
Volume
22
Issue
6
Pages
1349-1356
ISSN
  • 0953-816X (ISSN-L)
  • 1460-9568
OpenAlex
W2075127191
Cited by
52
References
56
Citations by year
2025: 2 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 2 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 2 · 2014: 1 · 2013: 2 · 2012: 3
FWCI
2.13
Type
journal article
Language
en
Open access
closed
Locations
  • European Journal of Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • National Institutes of Health
  • National Institute of Mental Health (MH61492, R01MH061492, MH600013)
  • National Institute on Drug Abuse (DA 16454, R01DA016454)
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
nicotine, nicotinic acetylcholine receptors, glutamatergic neurotransmission, hippocampal CA3, stratum lacunosum-moleculare, stratum radiatum, GABAergic interneurons, mecamylamine, methyllycaconitine, memory enhancement, cholinergic modulation, synaptic potentiation
MeSH terms
Aconitine, Animals, Dose-Response Relationship, Drug, Electric Stimulation, Glutamates, Hippocampus, Male, Mecamylamine, Synaptic Transmission, Neurons, Afferent, Nicotine, Receptors, Nicotinic, Rats, Sprague-Dawley, Nicotinic Agonists, Nicotinic Antagonists, GABA Antagonists, Excitatory Postsynaptic Potentials, Rats, In Vitro Techniques

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