Stress regulation of sustained attention and the cholinergic attention system
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ABSTRACT:
PROVIDER: PRJNA619064 | ENA |
REPOSITORIES: ENA
Dataset's files
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| SRR11458800_1.fastq.gz | Fastqsanger.gz | |||
| SRR11458800_2.fastq.gz | Fastqsanger.gz | |||
| SRR11458801_1.fastq.gz | Fastqsanger.gz | |||
| SRR11458801_2.fastq.gz | Fastqsanger.gz | |||
| SRR11458802_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Stress exacerbates symptoms of schizophrenia and attention deficit hyperactivity disorder, which are characterized by impairments in sustained attention. Yet how stress regulates attention remains largely unexplored. Here we investigated whether a 6-day variable stressor (VS) altered sustained attention and the cholinergic attention system in male and female rats. Methods: Sustained attention was tested with the sustained attention task (SAT). Successful performance on SAT relies on the release of acetylcholine (ACh) into the cortex from cholinergic neurons in the nucleus basalis of Meynert (NBM). Thus, we evaluated whether VS altered the morphology of these neurons with a novel approach using Cre-dependent virus in genetically modified ChAT::Cre rats, a species used for this manipulation only. Next, electrochemical recordings measured cortical ACh following VS. Finally, we used RNAseq to identify VS-induced transcriptional changes in the NBM. Results: VS impaired attentional performance in SAT and increased the dendritic complexity of NBM cholinergic neurons in both sexes. NBM cholinergic neurons are mainly under inhibitory control, so this morphological change could increase inhibition on these neurons, reducing downstream ACh release to impair attention. Indeed, VS decreased ACh release in the prefrontal cortex of males. Quantification of global transcriptional changes revealed that, although VS induced many sex-specific changes in gene expression, it increased several signaling molecules in both sexes.
2020-05-01 | GSE147806 | GEO
Project description:BackgroundStress exacerbates symptoms of schizophrenia and attention-deficit/hyperactivity disorder, which are characterized by impairments in sustained attention. Yet how stress regulates attention remains largely unexplored. We investigated whether a 6-day variable stressor altered sustained attention and the cholinergic attention system in male and female rats.MethodsSustained attention was tested with the sustained attention task. Successful performance on the sustained attention task relies on the release of acetylcholine (ACh) into the cortex from cholinergic neurons in the nucleus basalis of Meynert (NBM). Thus, we evaluated whether variable stress (VS) altered the morphology of these neurons with a novel approach using a Cre-dependent virus in genetically modified ChAT::Cre rats, a species used for this manipulation only. Next, electrochemical recordings measured cortical ACh following VS. Finally, we used RNA sequencing to identify VS-induced transcriptional changes in the NBM.ResultsVS impaired attentional performance in the sustained attention task and increased the dendritic complexity of NBM cholinergic neurons in both sexes. NBM cholinergic neurons are mainly under inhibitory control, so this morphological change could increase inhibition on these neurons, reducing downstream ACh release to impair attention. Indeed, VS decreased ACh release in the prefrontal cortex of male rats. Quantification of global transcriptional changes revealed that although VS induced many sex-specific changes in gene expression, it increased several signaling molecules in both sexes.ConclusionsThese studies suggest that VS impairs attention by inducing molecular and morphological changes in the NBM. Identifying mechanisms by which stress regulates attention may guide the development of novel treatments for psychiatric disorders with attention deficits.
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Project description:Acetylcholine (ACh) and its receptors (AChRs) are widely produced by various kinds of immune cells and fine-tune both innate and adaptive immune responses. However, whether cholinergic signaling regulates immune cell development is unclear. Here, we show that mouse CD4+CD8+ double-positive (DP) thymocytes express high levels of a9 nicotinic (n) AChR, and that this receptor controls the negative selection of thymocytes. Knock-out mice lacking a9 nAChR show an altered TCR repertoire and reduced CD4+ and CD8+ T cells in a mixed bone marrow chimera setting. Although thymic tuft cells, B cells, and a portion of T cells were all found to express choline acetyltransferase (ChAT) and so are sources of ACh in mouse thymus, T cell-derived ACh plays a more important regulatory role. Our results thus reveal a new mechanism of immune cell development control that involves lymphocyte-mediated cholinergic signaling.
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