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Specific loss of remote fear memory by knockdown of a neuron-specific nucleosome remodeling factor BAF53b in the amygdala

ABSTRACT: Specific loss of remote fear memory by knockdown of a neuron-specific nucleosome remodeling factor BAF53b in the amygdala

PROVIDER: PRJNA608858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11185016_1.fastq.gz	Fastqsanger.gz
	SRR11185016_2.fastq.gz	Fastqsanger.gz
	SRR11185017_1.fastq.gz	Fastqsanger.gz
	SRR11185017_2.fastq.gz	Fastqsanger.gz
	SRR11185018_1.fastq.gz	Fastqsanger.gz

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Specific loss of remote fear memory by knockdown of a neuron-specific nucleosome remodeling factor BAF53b in the amygdala

Project description:Despite recent advances, molecular events and mechanisms involved in long-lasting memory formation are unclear. Here, we report a critical role for nucleosome remodeling factor BAF53b in mice. We observed an increase of BAF53b expression beyond 24 h after fear conditioning in the lateral amygdala, which was crucial for memory retention at remote time. RNA-seq analyses and behavioral rescue experiments identified fibroblast growth factor-1 (FGF1) as a candidate downstream effector.

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Project description:Fear memory regulation is thought to be similar between humans and animals, and the role of stress in altering remote memory is little explored. Since individual variation in stress reactivity exists, should stress alter remote memory, invividuals with differing stress-reactivity would affect it to various degree. We evaluate this question using two strains of rats with differing stress-reactivity. The Fisher 344 (F344) strain is known to have active coping style and represent normal stress-reactivity, while the Wistar–Kyoto (WKY) rat shows passive coping strategies and heightened stress-reactivity. Male animals were exposed contextual fear conditioning (CFC) and four weeks later, chronic restraint stress (CRS) or no stress (NS) was administered for two weeks. Remote memory, immediate stress response to a second CFC, and reinstated fear memory was measured. Both recent and reinstated fear memory were greater in F344s, regardless of the stress status, In contrast, remote memory was attenuated in F344 only, concurring with their increased immediate stress responsive behavior after CRS. To find if this strain-specific response to CRS can be mirrored by transcriptomic changes in the blood, RNA sequencing was carried out. Overlapping differentially expressed genes (DEGs) between NS vs. CRS in the blood of F344 and WKY suggest a convergence of stress-related molecular mechanisms, independent of stress-reactivity. In contrast, DEGs unique to the F344 and the WKY stress responses are divergent in their functionality and networks, beyond that of strain differences in their non-stressed state. These unique DEGs than could be implicated as biomarkers stress-reactivity.

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