Cited by 17Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionGenetics and Neurodevelopmental Disorders

Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity

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Koesters, Andrew G., Rich, Mark M., Engisch, Kathrin L.·2024·The Neuroscientist

Abstract

The idea that the nervous system maintains a set point of network activity and homeostatically returns to that set point in the face of dramatic disruption—during development, after injury, in pathologic states, and during sleep/wake cycles—is rapidly becoming accepted as a key plasticity behavior, placing it alongside long-term potentiation and depression. The dramatic growth in studies of homeostatic synaptic plasticity of miniature excitatory synaptic currents (mEPSCs) is attributable, in part, to the simple yet elegant mechanism of uniform multiplicative scaling proposed by Turrigiano and colleagues: that neurons sense their own activity and globally multiply the strength of every synapse by a single factor to return activity to the set point without altering established differences in synaptic weights. We have recently shown that for mEPSCs recorded from control and activity-blocked cultures of mouse cortical neurons, the synaptic scaling factor is not uniform but is close to 1 for the smallest mEPSC amplitudes and progressively increases as mEPSC amplitudes increase, which we term divergent scaling. Using insights gained from simulating uniform multiplicative scaling, we review evidence from published studies and conclude that divergent synaptic scaling is the norm rather than the exception. This conclusion has implications for hypotheses about the molecular mechanisms underlying synaptic scaling.

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Crossref · 10.1177/10738584221112336

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  • Kv7 channels furnish a non-inactivating M-current that stabilizes the axon initial segment; redistribution or pharmacologic enhancement reduces spurious spiking and limits burst afterdepolarizations.

    “Kv7 channels furnish a non-inactivating M-current that stabilizes the axon initial segment; redistribution or pharmacologic enhancement reduces spurious spiking and limits burst afterdepolarizations [360,362].”

    From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [362]

    The sections on mEPSCs and global versus local signals discuss synaptic strength, Kir2.1, and activity-dependent spiking, not Kv7 channels. Searches for Kv7/M-current at the axon initial segment and for redistribution or enhancement affecting burst afterdepolarizations found no passage addressing the claim. Page numbers were not available in our copy. (LLM, conf=0.77)

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Authors
Koesters, A. G., Rich, M. M., & Engisch, K. L.
Affiliations
  • Wright-Patterson Air Force Base (US)
  • Wright State University (US)
Corresponding author
Engisch, Kathrin L.
Venue
The Neuroscientist
Published
2022-07-29
Volume
30
Issue
1
Pages
49-70
ISSN
  • 1073-8584 (ISSN-L)
  • 1089-4098
OpenAlex
W4288695827
Cited by
17
References
114
Citations by year
2026: 1 · 2025: 3 · 2024: 8 · 2023: 5
FWCI
0.57
Type
journal article
Language
en
Open access
Locations
  • The Neuroscientist (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • CORE Scholar (Wright State University) (submittedVersion)
  • Journal of Bioresource Management (submittedVersion, cc-by)
Funders
National Institute of Neurological Disorders and Stroke (P01 NS057228)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
homeostatic plasticity, miniature excitatory postsynaptic currents, synaptic scaling, cortical neurons, computer simulation
MeSH terms
Animals, Homeostasis, Neuronal Plasticity, Neurons, Synapses, Excitatory Postsynaptic Potentials, Mice

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