ArticleFrontiers in neuroanatomy2025
Selective vulnerability of stellate cells to gut dysbiosis: neuroanatomical changes in the medial entorhinal cortex.
Article in Frontiers in neuroanatomy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Parental microbiome programming of early-life neurodevelopment: multi-niche contributions through the microbiome-gut-brain axis.Gut microbes · 2026Review
- Human milk microbiome as a modulator of the early-life gut-brain axis: mechanisms and translational opportunities for neurodevelopment.Journal of translational medicine · 2026Review
- Gestational dysbiosis is associated with altered early-life microbial seeding and favors pathobiont expansion in offspring.iScience · 2026Article
- Maternal gut dysbiosis is associated with altered enteric and cortical inhibitory circuit development.Frontiers in neuroanatomy · 2026Article
- Harnessing the microbiota-gut-brain axis to prevent and treat pediatric neurodevelopmental disorders: translational insights and strategies.Journal of translational medicine · 2025Review
- The microbiota-gut-brain axis in mental and neurodegenerative disorders: opportunities for prevention and intervention.Frontiers in aging neuroscience · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
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Abstract
Introduction: The gut microbiota plays a critical role in regulating brain structure and function via the microbiota-gut-brain axis. Antibiotic-induced gut dysbiosis (AIGD) has been linked to neuroanatomical changes and cognitive deficits. However, its impact on neuronal morphology in layer II of the medial entorhinal cortex (mECII), a region central to spatial memory, remains poorly understood. This study examines how AIGD affects dendritic architecture in mECII stellate and pyramidal island cells. Methods: Mice received a broad-spectrum oral antibiotic cocktail to induce AIGD. Gut microbiota composition was analyzed using 16S rRNA sequencing. Golgi-stained neurons in mECII were assessed for dendritic complexity via Sholl analysis. Iba1 staining evaluated microglial activation in mECII. Intestinal sections were stained with NeuN and CD8 to assess enteric neuron density and inflammation. Microbial abundance was correlated with dendritic parameters. Results: AIGD resulted in significant dysbiosis, including depletion of butyrate-producing taxa ( Discussion: These findings suggest AIGD selectively alters mECII stellate cell morphology through peripheral immune signaling or microbial metabolites, independent of local microglial activation. This study highlights the role of gut microbiota in shaping neuronal architecture and supports microbiome-targeted strategies to counteract dysbiosis-associated neuroanatomical changes.
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