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High-frequency head impacts cause chronic synaptic adaptations and long-term cognitive impairment [Memantine study]

ABSTRACT: High-frequency head impacts cause chronic synaptic adaptations and long-term cognitive impairment [Memantine study]

PROVIDER: PRJNA695800 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13575851_1.fastq.gz	Fastqsanger.gz
	SRR13575851_2.fastq.gz	Fastqsanger.gz
	SRR13575852_1.fastq.gz	Fastqsanger.gz
	SRR13575852_2.fastq.gz	Fastqsanger.gz
	SRR13575853_1.fastq.gz	Fastqsanger.gz

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High-frequency head impacts cause chronic synaptic adaptations and long-term cognitive impairment [Memantine study]

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Project description:Shank2 is an excitatory postsynaptic scaffolding protein strongly implicated in autism spectrum disorders (ASD). Shank2-mutant mice with a homozygous deletion of exons 6 and 7 show decreased NMDA receptor (NMDAR) functions and autistic-like behaviors in juvenile (~postnatal day or P21) and adult (> P56) stages that are rescued by NMDAR activation. These mice, however, show an opposite change increased NMDAR functions—at ~P14, and NMDAR suppression by early and chronic memantine treatment during P7–21 prevents NMDAR hypofunction and autistic-like behaviors at juvenile (~P21) and adult (~P56) stages. To explore molecular mechanisms underlying the long-lasting effects of early memantine treatment, we performed RNA-Seq analysis of forebrains from wild-type and Shank2-mutant mice early and chronically treated with vehicle or memantine. Memantine-treated Shank2-mutant mice showed upregulations of chromatin-related genes and downregulations of mitochondria- and ribosome-related genes. In addition, vehicle-treated Shank2-mutant mice showed transcriptomic patterns that are largely opposite to those observed in ASD, as supported by the expression patterns of ASD-risk/related genes and cell-type-specific genes. These patterns, likely representing compensatory changes, were weakened by early memantine treatment. These results suggest that early chronic memantine treatment in Shank2-mutant mice alters chromatin- and mitochondria/ribosome-related gene expressions and weakens anti-ASD transcriptomic patterns.

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