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Seizure evolution in a mouse model of West syndrome involves complex and time-dependent 4 synapse remodeling, gliosis and alterations in lipid metabolism

ABSTRACT: To investigate molecular changes in the hippocampus of Cyfip2 Arg87Cys knock-in mice at the cell-type-specific manner, we conducted single-nucleus transcriptomic analysis at postnatal weeks 28.

ORGANISM(S): Mus musculus

PROVIDER: GSE293769 | GEO | 2025/09/24

REPOSITORIES: GEO

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Seizure evolution in a mouse model of West syndrome involves complex and time-dependent 4 synapse remodeling, gliosis and alterations in lipid metabolism

Project description:Seizure evolution in a mouse model of West syndrome involves complex and time-dependent 4 synapse remodeling, gliosis and alterations in lipid metabolism

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Brain transcriptome analysis in the cortex and hippocampus of Cyfip2 heterozygous mice at three different postnatal stages

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Brain transcriptome analysis in the cortex and hippocampus of Cyfip2 Arg87Cys knock-in mice at four different postnatal stages

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Stroke subtype-dependent synapse elimination by reactive gliosis in mice.

Project description:The pathological role of reactive gliosis in CNS repair remains controversial. In this study, using murine ischemic and hemorrhagic stroke models, we demonstrated that microglia/macrophages and astrocytes are differentially involved in engulfing synapses in the reactive gliosis region. By specifically deleting MEGF10 and MERTK phagocytic receptors, we determined that inhibiting phagocytosis of microglia/macrophages or astrocytes in ischemic stroke improved neurobehavioral outcomes and attenuated brain damage. In hemorrhagic stroke, inhibiting phagocytosis of microglia/macrophages but not astrocytes improved neurobehavioral outcomes. Single-cell RNA sequencing revealed that phagocytosis related biological processes and pathways were downregulated in astrocytes of the hemorrhagic brain compared to the ischemic brain. Together, these findings suggest that reactive microgliosis and astrogliosis play individual roles in mediating synapse engulfment in pathologically distinct murine stroke models and preventing this process could rescue synapse loss.

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Author Correction: Stroke subtype-dependent synapse elimination by reactive gliosis in mice.

Project description: Not available

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Deficiency of the neurodevelopmental disorder-associated gene Cyfip2 alters retinal ganglion cell properties and visual acuity

Project description:Intellectual disability (ID) is a neurodevelopmental disorder affecting approximately 0.5-3% of the population in the developed world. Individuals with ID exhibit deficits in intelligence and impaired adaptive behavior, frequently as well as visual impairments. Cytoplasmic FMR1-interacting protein 2 (CYFIP2) is an interacting partner of fragile X mental retardation protein, whose loss results in fragile X syndrome, the most common inherited cause of ID. Recently, CYFIP2 variants were found in patients with early-onset epileptic encephalopathy, developmental delay, and ID. Individuals with these CYFIP2 variants often exhibit visual impairments, however, the underlying mechanism is poorly understood. In the current study, we investigated the role of Cyfip2 in retinal and visual function by generating and analyzing mice in which Cyfip2 is depleted in the retina (Cyfip2 CKO mice). We found no major difference in the layer structure and cell composition between control and Cyfip2 CKO retinas, whereas a subset of genes associated with transporter and channel activity was differentially expressed in the Cyfip2 CKO retina. Multi-electrode array recordings showed more sustained and stronger response to positive flashes of ON ganglion cells in the Cyfip2 CKO retina, although we did not observe that Cyfip2 deficiency affects photoreceptor and ON bipolar cell functions by electroretinogram analysis. Furthermore, initial and late phase OKR analysis demonstrated that Cyfip2 deficiency impairs visual function at the organismal level. Together, our results shed light on the molecular mechanism underlying visual impairments observed in individuals with CYFIP2 variants and, more generally, in patients with neurodevelopmental disorders including ID.

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Project description:CYFIP2 is a component of the WAVE regulatory complex which regulates actin polymerization and branching in diverse cellular compartments. Recent molecular genetic studies identified mutations of CYFIP2 in patients with intellectual disability and seizures, suggesting that CYFIP2 may have some roles in brain development and function. To understand its functions in vivo at the molecular level, we performed RNA-seq analysis in juvenile Cyfip2 mutant mice.

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Prefrontal cortical transcriptome analysis of Cyfip2 mutant mice (adult mouse)

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