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Transcriptomic and neurochemical analysis of the stellate ganglia in mice highlights sex differences.

ABSTRACT: The stellate ganglia are the predominant source of sympathetic innervation to the heart. Remodeling of the nerves projecting to the heart has been observed in several cardiovascular diseases, however studies of adult stellate ganglia are limited. A profile of the baseline transcriptomic and neurochemical characteristics of the stellate ganglia in adult C57Bl6j mice, a common model for the study of cardiovascular diseases, may aid future investigations. We have generated a dataset of baseline measurements of mouse stellate ganglia using RNAseq, HPLC and mass spectrometry. Expression differences between male and female mice were identified. These differences included physiologically important genes for growth factors, receptors and ion channels. While the neurochemical profiles of male and female stellate ganglia were not different, minor differences in neurotransmitter content were identified in heart tissue.

SUBMITTER: Bayles RG

PROVIDER: S-EPMC5997635 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Transcriptomic and neurochemical analysis of the stellate ganglia in mice highlights sex differences.

Bayles R G RG Olivas A A Denfeld Q Q Woodward W R WR Fei S S SS Gao L L Habecker B A BA

Scientific reports 20180612 1

The stellate ganglia are the predominant source of sympathetic innervation to the heart. Remodeling of the nerves projecting to the heart has been observed in several cardiovascular diseases, however studies of adult stellate ganglia are limited. A profile of the baseline transcriptomic and neurochemical characteristics of the stellate ganglia in adult C57Bl6j mice, a common model for the study of cardiovascular diseases, may aid future investigations. We have generated a dataset of baseline mea ...[more]

PMID: 29895973

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Project description:BackgroundIn recent decades, increasing longevity (among other factors) has fostered a rise in Parkinson's disease incidence. Although not exhaustively studied in this devastating disease, the impact of sex represents a critical variable in Parkinson's disease as epidemiological and clinical features differ between males and females.MethodsTo study sex bias in Parkinson's disease, we conducted a systematic review to select sex-labeled transcriptomic data from three relevant brain tissues: the frontal cortex, the striatum, and the substantia nigra. We performed differential expression analysis on each study chosen. Then we summarized the individual differential expression results with three tissue-specific meta-analyses and a global all-tissues meta-analysis. Finally, results from the meta-analysis were functionally characterized using different functional profiling approaches.ResultsThe tissue-specific meta-analyses linked Parkinson's disease to the enhanced expression of MED31 in the female frontal cortex and the dysregulation of 237 genes in the substantia nigra. The global meta-analysis detected 15 genes with sex-differential patterns in Parkinson's disease, which participate in mitochondrial function, oxidative stress, neuronal degeneration, and cell death. Furthermore, functional analyses identified pathways, protein-protein interaction networks, and transcription factors that differed by sex. While male patients exhibited changes in oxidative stress based on metal ions, inflammation, and angiogenesis, female patients exhibited dysfunctions in mitochondrial and lysosomal activity, antigen processing and presentation functions, and glutamic and purine metabolism. All results generated during this study are readily available by accessing an open web resource ( http://bioinfo.cipf.es/metafun-pd/ ) for consultation and reuse in further studies.ConclusionsOur in silico approach has highlighted sex-based differential mechanisms in typical Parkinson Disease hallmarks (inflammation, mitochondrial dysfunction, and oxidative stress). Additionally, we have identified specific genes and transcription factors for male and female Parkinson Disease patients that represent potential candidates as biomarkers to diagnosis.

Project description:Alcohol-use disorders (AUDs) are characterized by repeated episodes of binge drinking. Based on reports that exposure to predator odor stress (PS) consistently increases ethanol intake, the present studies examined whether prior binge drinking differentially altered responsivity to PS and subsequent ethanol intake in male and female mice, when compared to mice without prior binge exposure. Initial studies in naïve male and female C57BL/6J mice confirmed that 30-min exposure to dirty rat bedding significantly increased plasma corticosterone (CORT) levels and anxiety-related behavior, justifying the use of dirty rat bedding as PS in the subsequent drinking studies. Next, separate groups of male and female C57BL/6J mice received seven binge ethanol sessions (binge) or drank water (controls), followed by a 1-month period of abstinence. Then, 2-bottle choice ethanol intake (10% or 10E vs. water, 23 h/day) was measured in lickometer chambers for 4 weeks. After baseline intake stabilized, exposure to intermittent PS (2×/week × 2 weeks) significantly enhanced ethanol intake after the 2nd PS in male, but not female, binge mice vs. baseline and vs. the increase in controls. However, in a subgroup of females (with low baselines), PS produced a similar increase in 10E intake in control and binge mice vs. baseline. Analysis of lick behavior determined that the enhanced 10E intake in binge male mice and in the female low baseline subgroup was associated with a significant increase in 10E bout frequency and 10E licks throughout the circadian dark phase. Thus, PS significantly increased 10E intake and had a synergistic interaction with prior binge drinking in males, whereas PS produced a similar significant increase in 10E intake in the low baseline subgroup of binge and control females. Plasma CORT levels were increased significantly in both binge and control animals after PS. CORT levels at 24-h withdrawal from daily 10E intake were highest in the groups with elevated 10E licks (i.e., binge males and control females). At 24-h withdrawal, protein levels of GABAA receptor α1 subunit, corticotropin releasing factor receptor 1, and glucocorticoid receptor in prefrontal cortex (PFC) and hippocampus (HC) were differentially altered in the male and female mice vs. levels in separate groups of age-matched naïve mice, with more changes in HC than in PFC and in females than in males. Importantly, the sexually divergent changes in protein levels in PFC and HC add to evidence for sex differences in the neurochemical systems influenced by stress and binge drinking, and argue for sex-specific pharmacological strategies to treat AUD.

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Transcriptomic and neurochemical analysis of the stellate ganglia in mice highlights sex differences.

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Transcriptomic and neurochemical analysis of the stellate ganglia in mice highlights sex differences.

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