ArticleCNS neuroscience & therapeutics2025
Liver X Receptor Beta Regulates Glial Dynamics and Cortical Network Remodeling in a Freezing Lesion-Cortical Dysplasia Model.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Liver X Receptor Beta Regulates Glial Dynamics and Cortical Network Remodeling in a Freezing Lesion-Cortical Dysplasia Model.CNS neuroscience & therapeutics · 2025Article
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12 authors.
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Abstract
backgroundFocal cortical dysplasia (FCD) is a leading cause of drug-resistant epilepsy, characterized by cortical malformations and aberrant neuronal-glial interactions. Recently, the role of Liver X Receptor Beta (LXRβ) in neurodevelopment has attracted considerable attention, although its involvement in FCD pathogenesis remains unclear.
methodsWe established a freezing lesion-cortical dysplasia (FL-CD) model in neonatal mice to mimic the pathological features of FCD. We evaluated the expression of LXRβ and its downstream target, brain lipid-binding protein (BLBP), using immunohistochemistry and Western blot analysis. LXRβ activation and inhibition were pharmacologically modulated to assess their effects on glial migration, differentiation and cortical electrophysiology. Electroencephalogram (EEG) recordings were analyzed for power spectral density and functional connectivity to further investigate alterations in cortical network activity.
resultsLXRβ and BLBP were significantly downregulated in the lesion cortex during early developmental stages. Activation of LXRβ reduced gliosis, promoted astrocytic differentiation, and modified cortical oscillatory activity, as evidenced by enhanced α power and gamma band functional connectivity, along with adjustments in the theta/beta ratio. In contrast, inhibition of LXRβ exacerbated gliosis and disrupted cortical network synchronization.
conclusionOur findings demonstrate that LXRβ plays a critical role in regulating glial migration, differentiation and cortical network remodeling in the FL-CD model. Pharmacological modulation of LXRβ may offer a novel therapeutic strategy for restoring neural circuit stability in FCD, highlighting its potential as a molecular target for intervention in drug-resistant epilepsy.
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