ArticleFrontiers in cell and developmental biology2025
Astrocytic gatekeeping of neural circuitry and synaptic balance in an autism mouse model: mechanistic insights beyond
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Autism spectrum disorder (ASD) is characterized by impaired synaptic development and disrupted excitation/inhibition (E/I) balance. While neuronal mechanisms have been extensively studied, accumulating evidence indicates that glial cells-particularly astrocytes-play a crucial role in maintaining synaptic homeostasis and regulating neurotransmission during brain development. However, the functional contribution of astrocytes to ASD pathogenesis remains insufficiently defined. Methods: This study aimed to explore astrocyte-mediated regulation of E/I balance in ASD using Results: Gb extract reversed VPA-induced alterations in neural progenitor proliferation and differentiation and restored expression of key synaptic proteins (neuroligins, neurexin, synaptophysin). Notably, astrocyte-specific markers (GFAP, EAAT1/2) and E/I-related transporters (vGluT1, VGAT, GABA R1α, NMDA R1) were dysregulated in the ASD model and normalized by Gb treatment. Co-culture experiments demonstrated that astrocytes from VPA-treated animals, rather than neurons alone, were primarily responsible for E/I imbalance and synaptic abnormalities. Gb extract acted as a modulator of astrocytic function, restoring synaptic integrity and neurodevelopmental stability. Conclusion: Our findings underscore the pivotal role of astrocytes in the development and modulation of ASD-related synaptic pathology. Gb extract served as a valuable biological tool to reveal glial contributions to synaptic regulation and E/I balance. These insights support targeting astrocytic pathways with Gb extract as a novel therapeutic strategy for ASD.
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