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Cited by 253Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchNeural dynamics and brain function

Distributed Network Actions by Nicotine Increase the Threshold for Spike-Timing-Dependent Plasticity in Prefrontal Cortex

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Couey, Jonathan J., Meredith, Rhiannon M., Spijker, Sabine, Poorthuis, Rogier B., Smit, August B., Brussaard, Arjen B., Mansvelder, Huibert D.·2007·Neuron
DOI 10.1016/j.neuron.2007.03.006
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Abstract

Nicotine enhances attention and working memory by activating nicotinic acetylcholine receptors (nAChRs). The prefrontal cortex (PFC) is critical for these cognitive functions and is also rich in nAChR expression. Specific cellular and synaptic mechanisms underlying nicotine's effects on cognition remain elusive. Here we show that nicotine exposure increases the threshold for synaptic spike-timing-dependent potentiation (STDP) in layer V pyramidal neurons of the mouse PFC. During coincident presynaptic and postsynaptic activity, nicotine reduces dendritic calcium signals associated with action potential propagation by enhancing GABAergic transmission. This results from a series of presynaptic actions involving different PFC interneurons and multiple nAChR subtypes. Pharmacological block of nAChRs or GABA(A) receptors prevented nicotine's actions and restored STDP, as did increasing dendritic calcium signals with stronger postsynaptic activity. Thus, by activating nAChRs distributed throughout the PFC neuronal network, nicotine affects PFC information processing and storage by increasing the amount of postsynaptic activity necessary to induce STDP.

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  • In layer V pyramidal neurons, activation of presynaptic β2* nAChRs on thalamic glutamatergic inputs strongly enhances neuronal activity.

    “In contrast, in layer V pyramidal neurons, activation of presynaptic β2* nAChRs on glutamatergic inputs from the thalamus strongly enhances activity of these neurons (Gioanni et al. 1999; Lambe et al. 2003; Couey et al. 2007; Poorthuis et al. 2012).”

    From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Couey et al. 2007

    The Discussion (page not provided) says that β2-containing nAChRs on thalamic glutamatergic fibers projecting to layer V pyramidal neurons respond to activation. It also says these receptors are most likely not on presynaptic glutamatergic terminals. The Direct Nicotinic Actions section reports increased spontaneous excitatory transmission to pyramidal neurons, but does not establish that thalamic input strongly enhances the neurons’ activity. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • The nicotine-induced shift in prefrontal network activity may affect plasticity and refinement of cortical connections.

    “This may affect plasticity and refinement of cortical connections (Couey et al. 2007)”

    From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Couey et al. 2007

    The Abstract (page not supplied) reports that nicotine raises the threshold for spike-timing-dependent synaptic potentiation in mouse prefrontal cortex, supporting an effect on plasticity. The Discussion describes possible effects on prefrontal network processing, but does not address refinement of cortical connections. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Nicotine in mPFC changes the rules for spike-timing-dependent plasticity and thereby prevents synaptic potentiation.

    “In addition, nicotine in the mPFC changes the rules for spike-timing-dependent plasticity and thereby prevents synaptic potentiation (34).”

    From Adolescent nicotine exposure transiently increases high-affinity nicotinic receptors and modulates inhibitory synaptic transmission in rat medial prefrontal cortex (2012) · cites this paper as [34]

    The Results section reports that nicotine prevented potentiation when presynaptic input was paired with a single postsynaptic action potential, and the Discussion says nicotine raises the threshold for spike-timing-dependent plasticity. But the paper also reports that stronger postsynaptic activity can partially restore potentiation, so nicotine does not prevent it categorically. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The majority of interneurons express nAChRs composed of α4β2*, although they also express other subunits.

    “the majority of interneurons express nAChRs that are composed of α4β2*, although they also express other subunits (34)”

    From Adolescent nicotine exposure transiently increases high-affinity nicotinic receptors and modulates inhibitory synaptic transmission in rat medial prefrontal cortex (2012) · cites this paper as [34]

    In “Different Types of Interneurons Differentially Express mRNA for nAChRs” (Table 1), the paper reports α4 expression in the largest number of LTS and RSNP cells, with β2 and α7 mRNA also found in those cell types. It also reports hardly any nAChR-subunit mRNA in FS cells. These findings support expression of several subunits in some interneuron types, but do not establish that a majority of interneurons express assembled α4β2* receptors. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Increased inhibition can block long-term potentiation induction in the hippocampus and raise the threshold for spike-timing-dependent plasticity.

    “Increased inhibition can lead to blockade of long-term potentiation (LTP) induction in the hippocampus (Ji et al. 2001) and increase in the threshold for induction of spike-timing-dependent plasticity (STDP) (Couey et al. 2007).”

    From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Couey et al. 2007

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Authors
Couey, J. J., Meredith, R. M., Spijker, S., Poorthuis, R. B., Smit, A. B., Brussaard, A. B., & Mansvelder, H. D.
Affiliations
Vrije Universiteit Amsterdam (NL)
Corresponding author
Mansvelder, Huibert D.
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2007-04
Volume
54
Issue
1
Pages
73-87
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2007.03.006
OpenAlex
W2077516679
Cited by
253
References
68
Citations by year
2026: 2 · 2025: 8 · 2024: 5 · 2023: 9 · 2022: 9 · 2021: 13 · 2020: 5 · 2019: 14 · 2018: 18 · 2017: 15 · 2016: 11 · 2015: 12 · 2014: 21 · 2013: 22 · 2012: 18
FWCI
7.21
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • VU Research Portal (publishedVersion, other-oa)
  • Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
Funders
  • Koninklijke Nederlandse Akademie van Wetenschappen
  • ZonMw
  • Medical Research Council
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 › Neural dynamics and brain function
Keywords
nicotine, nicotinic acetylcholine receptors, spike-timing-dependent plasticity, prefrontal cortex, layer 5 pyramidal neurons, GABAergic neurotransmission, GABAA receptor, presynaptic inhibition, nAChR subtypes, working memory, attention
MeSH terms
Action Potentials, Animals, Animals, Newborn, Drug Interactions, Mice, Inbred C57BL, Models, Neurological, Nerve Net, Neuronal Plasticity, Neurons, Nicotine, Reaction Time, Receptors, Nicotinic, Prefrontal Cortex, Nicotinic Agonists, GABA Antagonists, Excitatory Postsynaptic Potentials, Calcium Signaling, Reverse Transcriptase Polymerase Chain Reaction, Mice, In Vitro Techniques

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