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The histone lysine demethylase KDM7A contributes to reward memory via Fscn1-induced synaptic plasticity in the medial prefrontal cortex

ABSTRACT: The histone lysine demethylase KDM7A contributes to reward memory via Fscn1-induced synaptic plasticity in the medial prefrontal cortex

PROVIDER: PRJNA1158768 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30610065_1.fastq.gz	Fastqsanger.gz
	SRR30610066_1.fastq.gz	Fastqsanger.gz
	SRR30610067_1.fastq.gz	Fastqsanger.gz
	SRR30610068_1.fastq.gz	Fastqsanger.gz
	SRR30610069_1.fastq.gz	Fastqsanger.gz

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The histone lysine demethylase KDM7A contributes to reward memory via Fscn1-induced synaptic plasticity in the medial prefrontal cortex

Project description:Lysine demethylase 7A (KDM7A) catalyzes the removal of dimethylation from histone H3 lysine 9 and lysine 27, both of which are associated with transcription repression. Previous study indicated that Kdm7a mRNA in the medial prefrontal cortex (mPFC) increased after drug exposure, yet its role in drug-related behaviors is largely unknown. In a morphine-conditioned place preference (CPP) paradigm, our findings revealed a specific increase of Kdm7a expression in the mPFC seven days after drug withdrawal. Subsequently, our results demonstrated that knockdown of Kdm7a in the mPFC did not affect the acquisition of morphine-induced CPP, but it attenuated memory consolidation. To further explore Kdm7a-mediated transcriptomic changes, we employed Nanopore direct RNA sequencing. Transcriptome profiling unveiled several gene expression alterations impacted by KDM7A, which were enriched in relevant neural function categories. Notably, we identified and validated fascin actin-bundling protein 1 (Fscn1) as a downstream molecular target. Knockdown of Fscn1 had a similar impact on CPP to Kdm7a, along with a corresponding decrease in dendritic spine density in the mPFC. Additionally, ChIP analysis demonstrated that silencing Kdm7a in N2a cells resulted in decreased enrichment of H3K9me2 and H3K27me2 at the Fscn1 promoter region, suggesting that Kdm7a may act as a crucial regulator of transcriptional responses to morphine-related reward memory via Fscn1.

2025-03-19 | GSE276730 | GEO

The Histone Lysine Demethylase KDM7A Contributes to Reward Memory via Fscn1-Induced Synaptic Plasticity in the Medial Prefrontal Cortex.

Project description:Lysine demethylase 7A (KDM7A) catalyzes the removal of dimethylation from histone H3 lysine 9 and lysine 27, both of which are associated with transcription repression. Previous study indicates that Kdm7a mRNA in the medial prefrontal cortex (mPFC) increases after drug exposure, yet its role in drug-related behaviors is largely unknown. In a morphine-conditioned place preference (CPP) paradigm, these findings reveal a specific increase of Kdm7a expression in the mPFC 7 days after drug withdrawal. Subsequently, these results demonstrate that knockdown of Kdm7a in the mPFC do not affect the acquisition of morphine-induced CPP, but it attenuate memory consolidation. To further explore Kdm7a-mediated transcriptomic changes, this work employs Nanopore direct RNA sequencing. Transcriptome profiling unveils several gene expression alterations impacted by KDM7A, which are enriched in relevant neural function categories. Notably, this work identifies and validates fascin actin-bundling protein 1 (Fscn1) as a downstream molecular target. Knockdown of Fscn1 has a similar impact on CPP to Kdm7a, along with corresponding decrease of dendritic spine density and neuronal activity in the mPFC. Additionally, silencing Kdm7a decreases enrichment of H3K9me2 and H3K27me2 at the Fscn1 promoter region, suggesting that KDM7A may act as a crucial regulator of transcriptional responses to morphine-related reward memory via Fscn1.

| S-EPMC11905110 | biostudies-literature

Transcriptomic analysis of prefrontal medial cortex, hippocampus and nucleus accumbens of alcohol-preferring and nonpreferring rats

Project description:Animal models provide opportunity to study neurobiological aspects of human alcoholism. Changes in gene expression have been implicated in mediating brain function, including reward system and addiction. The current study aimed to identify novel genes that may underlie ethanol preference. Microarray analysis comparing gene expression in nucleus accumbens (NAc), hippocampus (HP) and prefrontal medial cortex (mPFC) was performed in two rat strains selected for extreme levels of ethanol preference - Warsaw High Preferring (WHP) and Warsaw Low Preferring (WLP). The identified candidate genes may underlie differential ethanol preference in rat model of alcoholism. This is analysis of 18 RNA samples, including 9 technical replicates. Two strains of rats selected for extreme levels of ethanol preference (low preferring WLP and high preferring WHP) were compared. Three brain areas (nucleus accumbens, prefrontal medial cortex and hippocampus) were studied. For each brain area, 6 RNA samples (including 3 technical replicates) were analyzed. Each RNA sample consist of of equal amounts of total RNA from 3 male rats. Comparisons: Nucleus accumbens of WHP vs. Nucleus accumbens of WLP; Prefrontal medial cortex of WHP vs. Prefrontal medial cortex of WLP; Hippocampus of WHP vs. Hippocampus of WLP. 3 biological replicates in each comparison.

2015-01-17 | E-GEOD-65064 | biostudies-arrayexpress

Brief exposure to oral antibiotics has age-dependent effects on morphine reward and gene expression in the medial prefrontal cortex of adolescent and adult mice_1

Project description:Adolescence is a critical period for the initiation of problematic drug use, which significantly increases the risk of developing substance use disorders later in life. This heightened vulnerability is partly attributed to the immaturity of the prefrontal cortex, a brain region both essential for decision-making and implicated in drug reward. During adolescence, peripheral systems, such as the gut microbiome, also undergo substantial changes. Emerging evidence suggests that disruptions to the gut microbiome can influence gene expression and drug reward behaviors in rodent models. In this study, we investigated the effects of oral antibiotics on morphine reward and prefrontal cortical gene expression in adolescent and adult mice. Using oral antibiotics to transiently disrupt the microbiome, we found that short-term antibiotic exposure reduced morphine place preference specifically in adolescent mice. In a separate cohort, we observed that antibiotic treatment altered the transcriptomic response to morphine in the medial prefrontal cortex across all age groups. Notably, the transcriptomic changes induced by antibiotics and morphine were age-specific, with distinct gene expression patterns observed in adolescents compared to adults. These findings establish a foundation for future research into the role of the gut microbiome in opioid reward and highlight potential gene pathways underlying age-dependent differences in opioid sensitivity.

2025-08-01 | GSE303730 | GEO

Juvenile fluoxetine evoked gene expression changes in the rat medial prefrontal cortex

Project description:To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.

2024-06-30 | GSE270731 | GEO

Postnatal fluoxetine evoked gene expression changes in the rat medial prefrontal cortex

Project description:To understand the consequences of chronic exposure to fluoxetine during postnatal life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during postnatal life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.

2024-06-30 | GSE270730 | GEO

Transcriptomic analysis of prefrontal medial cortex, hippocampus and nucleus accumbens of alcohol-preferring and nonpreferring rats

2015-01-17 | GSE65064 | GEO

Proteomic characterization of the medial prefrontal cortex in chronic restraint stress mice

Project description:In this study, we used chronic restraint stress to establish a mouse model of depression, and differentially expressed proteins in the medial prefrontal cortex of depressive model mice were detected by TMT proteomics. By functional enrichment analysis of the differentially expressed proteins, we found that CRS-induced mice have altered synaptic function and excessive autophagy. In addition, we also demonstrated that CRS may disrupt synaptic plasticity by affecting activation of the Wnt2b/尾-catenin pathway which may help explain the pathogenesis of depression and identify new antidepressant drug targets.

2024-08-27 | PXD054244 | Pride

Gene expression microarray analysis on the medial prefrontal cortex of wild-type mice (2W and 12W)

Project description:The gene expression patterns in the medial prefrontal cortex of wild-type mice (2W and 12W) were examined using Affymetrix GeneChip arrays.

2019-02-25 | GSE118667 | GEO

Gene expression microarray analysis on the medial prefrontal cortex of Camk2a+/- mice and wild-type mice

Project description:The gene expression patterns in the medial prefrontal cortex of Camk2a+/- mice and wild-type mice were examined using Affymetrix GeneChip arrays.

2019-02-25 | GSE118724 | GEO

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