ArticleBMC biology2025
Ectopic expression of Slc1a2 in the prefrontal cortex of sleep-deprived male mice counteracts the glutamate/GABA-glutamine dysfunction.
Article in BMC biology, 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.
- Integration of transcriptome and DNA methylation reveals the mechanism of cilia-related genes in recurrent miscarriage.Scientific reports · 2026Article
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14 authors.
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Abstract
backgroundThe prefrontal cortex (PFC) plays a pronounced role in cognitive and emotional functions, which may be compromised by dismal sleep quality. This study intended to clarify the impact of Slc1a2 ectopic expression in the PFC on sleep deprivation (SD)-induced disturbances in the glutamate (Glu)/GABA-glutamine cycle and the role of astrocyte (AC)-neuron (Neu) communication.
methodsSingle-cell RNA sequencing was adopted to illuminate cell-specific changes in the brainstem, cortex, and hypothalamus of mice under NS, SD, and post-SD conditions. Cell communication analysis was applied to study interactions between ACs and Neus, which altered after the SD. Slc1a2 was ectopically expressed in the PFC and subjected to SD, followed by electrophysiological, immunofluorescence staining, and [
resultsSD caused notable changes in cellular distribution and downregulation of metabolic and synaptic genes in affected brain regions. Cell communication studies highlighted a reduction in AC-Neu interactions, with corresponding metabolic disruptions in the Glu/GABA-glutamine cycle as depicted by [
conclusionsSlc1a2 ectopic expression in the PFC negates SD-induced GABA dysfunction through vital AC-Neu communication. This study sheds light on the mechanisms through which SD affects neural function and suggesting potential treatments for sleep-related disorders.
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