Glial 5-HT signaling enables experience-dependent synapse remodeling in Drosophila and mammalian models.
This systematic review synthesizes foundational work from Drosophila and mammalian models to investigate the roles of glial 5-HT signaling in brain circuit plasticity. The analysis contrasts these mechanisms against neuron-only models and global serotonin elevation strategies. The study population encompasses Drosophila and mammalian models, with specific focus on glial infiltration and extracellular matrix remodeling processes.
The review reports that glial 5-HT signaling, alongside 5-HT2A receptor activation and matrix metalloprotease-mediated function, allows access for experience-driven synapse elimination. This targeted induction can re-open critical period-like synapse pruning even at maturity. In contrast, disruption of serotonergic regulation is proposed to contribute to a spectrum of neurodevelopmental disorders, including Fragile X syndrome, though these are based on model observations rather than human clinical data.
Safety considerations highlight the importance of avoiding the negative side effects associated with global serotonin elevation. The review notes that while enabling large-scale connectivity changes has broad potential therapeutic applications for disease, injury, trauma, and cognitive dysfunction, the evidence is derived from preclinical models. Limitations include the lack of reported absolute numbers, p-values, or specific effect sizes, as well as the absence of reported follow-up data or human safety profiles.
The practice relevance suggests that understanding glial contributions to synaptic remodeling could inform future therapeutic strategies. However, clinicians should interpret these findings as mechanistic insights from model systems rather than direct evidence for human treatment. The review does not report specific adverse events or discontinuations, as these outcomes were not applicable to the non-human study designs.
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