Cited by 38Neuroscience and Neuropharmacology ResearchIon channel regulation and functionNeural dynamics and brain function

The contribution of ion channels in input-output plasticity

Open access
Debanne, Dominique, Russier, Michaël·2019·Neurobiology of Learning and Memory

Abstract

Persistent changes that occur in brain circuits are classically thought to be mediated by long-term modifications in synaptic efficacy. Yet, many studies have shown that voltage-gated ion channels located at the input and output side of the neurons are also the subject to persistent modifications. These channels are thus responsible for intrinsic plasticity that is expressed in many different neuronal types including glutamatergic principal neurons and GABAergic interneurons. As for synaptic plasticity, activation of synaptic glutamate receptors initiate persistent modification in neuronal excitability. We review here how synaptic input can be efficiently altered by activity-dependent modulation of ion channels that control EPSP amplification, spike threshold or resting membrane potential. We discuss the nature of the learning rules shared by intrinsic and synaptic plasticity, the mechanisms of ion channel regulation and the impact of intrinsic plasticity on induction of synaptic modifications.

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Crossref · 10.1016/j.nlm.2019.107095

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  • Chronic stress induces cell-type-specific shifts in intrinsic excitability within medial prefrontal and hippocampal neurons, biasing circuits toward vulnerability or resilience depending on channel composition and neuromodulatory state.

    “Chronic stress induces cell-type-specific shifts in intrinsic excitability within medial prefrontal and hippocampal neurons, biasing circuits toward vulnerability or resilience depending on channel composition and neuromodulatory state [25,26].”

    From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [25]

    The sections on homeostatic plasticity and GABAergic interneurons describe cell-type-dependent changes in intrinsic excitability involving ion channels, including in hippocampal neurons. They discuss activity deprivation and synaptic stimulation, not chronic stress; the passages do not establish shifts in medial prefrontal neurons or a resulting bias toward vulnerability or resilience. (LLM, conf=0.84)

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  • Intrinsic excitability regulates neuronal gain and input-output transformations at the single cell level, unlike synaptic plasticity which modifies connection efficacy.

    “Unlike synaptic plasticity, which modifies the efficacy of connections between neurons, intrinsic excitability regulates neuronal gain and input–output transformations at the single cell level [24,25,26].”

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Authors
Debanne, D., & Russier, M.
Affiliations
Inserm (FR)
Corresponding author
Debanne, Dominique
Venue
Neurobiology of Learning and Memory
Publisher
Elsevier BV
Published
2019-12
Volume
166
Pages
107095
ISSN
1074-7427 (ISSN-L)
OpenAlex
W2974430957
Cited by
38
References
108
Citations by year
2026: 3 · 2025: 5 · 2024: 14 · 2023: 6 · 2022: 1 · 2021: 7 · 2020: 2
FWCI
0.33
Type
journal article
Language
en
Open access
Locations
  • Neurobiology of Learning and Memory (acceptedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
Funders
Institut National de la Santé et de la Recherche Médicale
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
intrinsic plasticity, ion channels, synaptic plasticity, voltage-gated ion channels, neuronal excitability, GABAergic interneurons, spike threshold, resting membrane potential, learning rules, ion channel modulation
MeSH terms
Action Potentials, Animals, Brain, Ion Channels, Learning, Memory, Synaptic Transmission, Neuronal Plasticity, Neurons

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