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Scn2a deletion disrupts oligodendroglia function: Implication for myelination, neural circuitry, and auditory hypersensitivity in ASD.

ABSTRACT: Scn2a deletion disrupts oligodendroglia function: Implication for myelination, neural circuitry, and auditory hypersensitivity in ASD.

PROVIDER: PRJNA1058459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27372616_1.fastq.gz	Fastqsanger.gz
	SRR27372616_2.fastq.gz	Fastqsanger.gz

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Scn2a deletion disrupts oligodendroglia function: Implication for myelination, neural circuitry, and auditory hypersensitivity in ASD.

Project description:Autism spectrum disorder (ASD) is characterized by a complex etiology, with genetic determinants significantly influencing its manifestation. Among these, the Scn2a gene emerges as a pivotal player, crucially involved in oligodendrocyte (OL) function. The present study elucidates the underexplored roles of Scn2a in OL functionality, subsequently affecting myelination and auditory neural processes. The results reveal a nuanced interplay between OLs and axons, where Scn2a deletion causes alterations in OL differentiation and myelination. This disruption, in turn, instigates changes in axonal properties and neuronal activities at the single cell level. Furthermore, OL-specific Scn2a deletion compromises the integrity of neural circuitry within auditory pathways, leading to auditory hypersensitivity—a common sensory abnormality observed in ASD. Through transcriptional profiling, we identified alterations in the expression of myelin-associated genes, highlighting the cellular consequences engendered by Scn2a deletion. In summary, the findings of this study provide unprecedented insights into the pathway from Scn2a deletion in OL to sensory abnormalities in ASD, underscoring the integral role of Scn2a-mediated OL myelination in auditory responses. This research thereby provides novel insights into the intricate tapestry of genetic and cellular interactions inherent in ASD.

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