Tau reduction affects excitatory and inhibitory neurons differently, reduces excitation/inhibition ratios, and counteracts network hypersynchrony
Open accessAbstract
The protein tau has been implicated in many brain disorders. In animal models, tau reduction suppresses epileptogenesis of diverse causes and ameliorates synaptic and behavioral abnormalities in various conditions associated with excessive excitation-inhibition (E/I) ratios. However, the underlying mechanisms are unknown. Global genetic ablation of tau in mice reduces the action potential (AP) firing and E/I ratio of pyramidal cells in acute cortical slices without affecting the excitability of these cells. Tau ablation reduces the excitatory inputs to inhibitory neurons, increases the excitability of these cells, and structurally alters their axon initial segments (AISs). In primary neuronal cultures subjected to prolonged overstimulation, tau ablation diminishes the homeostatic response of AISs in inhibitory neurons, promotes inhibition, and suppresses hypersynchrony. Together, these differential alterations in excitatory and inhibitory neurons help explain how tau reduction prevents network hypersynchrony and counteracts brain disorders causing abnormally increased E/I ratios.
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Tau can regulate PI3K-Akt-mTOR signaling, but under pathological stress such as in ASD or amyloid accumulation, it can promote network dysfunction.
“Tau can regulate this pathway [56], but under pathological stress such as in conditions such as ASD or amyloid accumulation, it can promote network dysfunction [22, 143].”
From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [22]
Endogenous tau likely contributes to network hyperexcitability across primary and secondary epilepsies.
“Given tau’s role in modulating neuronal activity under normal physiological conditions (DeVos et al., 2013; Chang et al., 2021), endogenous tau likely contributes to network hyperexcitability across primary and secondary epilepsies.”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Chang et al., 2021
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“Given tau’s role in modulating neuronal activity under normal physiological conditions (DeVos et al., 2013; Chang et al., 2021), endogenous tau likely contributes to network hyperexcitability across primary and secondary epilepsies.”
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- Authors
- Chang, C.-W., Evans, M. D., Yu, X., Yu, G.-Q., & Mucke, L.
- Affiliations
- Gladstone Institutes (US)
- Corresponding author
- Mucke, Lennart
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2021-10
- Volume
- 37
- Issue
- 3
- Pages
- 109855
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC8648275
- OpenAlex
- W3206269001
- Cited by
- 81
- References
- 66
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 17 · 2023: 18 · 2022: 17
- FWCI
- 6.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute of Mental Health (R01MH115679)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- tau protein, inhibitory interneurons, pyramidal neurons, axon initial segment, neuronal excitability, epileptogenesis, homeostatic plasticity, overstimulation, cortical slices, primary neuronal cultures
- MeSH terms
- Alzheimer Disease, Animals, Cells, Cultured, Epilepsy, Female, Interneurons, Male, Mice, Inbred C57BL, Neural Inhibition, Neural Pathways, Neuronal Plasticity, Somatosensory Cortex, Time Factors, tau Proteins, Pyramidal Cells, Mice, Knockout, Excitatory Postsynaptic Potentials, Mice, Inhibitory Postsynaptic Potentials, Mice, 129 Strain
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