The acute stress response is mediated by prefrontal 5α-reductase 2 in males via allopregnanolone synthesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1111852 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29040900.fastq.gz | Fastqsanger.gz | |||
| SRR29040901.fastq.gz | Fastqsanger.gz | |||
| SRR29040902.fastq.gz | Fastqsanger.gz | |||
| SRR29040903.fastq.gz | Fastqsanger.gz | |||
| SRR29040904.fastq.gz | Fastqsanger.gz |
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Project description:Acute stress triggers rapid brain responses, including increased allopregnanolone (AP) synthesis via 5α-reductase (5αR). However, the involvement of this enzyme in stress response remains elusive. Here, we investigated the roles of the two major 5αR isoenzymes in acute stress. Acute stress increased mRNA and protein levels of 5αR2, but not 5αR1, in the medial prefrontal cortex (mPFC) of male, but not female, rats. Targeted mPFC downregulation of 5αR2, but not 5αR1, markedly reduced the responsiveness of males, but not females, to both stressful and arousing stimuli. Similar sex differences were observed in 5αR2 knockout rats. While 5αR1 regulated AP synthesis under baseline conditions, 5αR2 enabled this process in response to acute stress. Single-nucleus transcriptomic analyses revealed that 5αR2 enabled stress-induced protein synthesis in pyramidal neurons and glia of the mPFC. These findings underscore the pivotal role of 5αR2 in shaping sex-related differences in acute stress reactivity.
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Project description:Background: The present study investigated a role of proteins from BET family (epigenetic readers) in schizophrenia-like abnormalities in MAM-E17 model of schizophrenia. Methods: An inhibitor of BET proteins, JQ1, was given during adolescence in postnatal days (P) 23-P30, and behavioral response (sensorimotor gating, recognition memory) and prefrontal cortex (mPFC) function (long-term potentiation (LTP), molecular and proteomic studies) were performed in adult males and females. Results: Deficits in sensorimotor gating and recognition memory were observed only in MAM-treated males. However, adolescent JQ1 treatment affected control, but MAM-treated groups in both sexes. Electrophysiological study showed an LTP impairment only in male MAM-treated animals, and JQ1 did not have any effect on LTP in the mPFC. In contrast, MAM did not affect immediate early gene expression (markers of neuronal and synaptic activity), but JQ1 altered them in both sexes. Proteomic study revealed alterations in MAM-treated groups only in males, while JQ1 affected both sexes. Conclusions: Prenatal MAM administration induced schizophrenia-like abnormalities only in males. In contrast, adolescent JQ1 treatment affected both sexes and induced behavioral changes in control groups, altered a markers of neuronal and synaptic activity and proteomic landscape in the mPFC of both groups (VEH- and MAM-treated). Thus, adolescent inhibition of BET family might change neuroplasticity in the mPFC.
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