iBet uBet web content aggregator. Adding the entire web to your favor.
iBet uBet web content aggregator. Adding the entire web to your favor.



Link to original content: http://pubmed.ncbi.nlm.nih.gov/38977070/
Subregion-specific transcriptomic profiling of rat brain reveals sex-distinct gene expression impacted by adolescent stress - PubMed Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2024 Aug 16:553:19-39.
doi: 10.1016/j.neuroscience.2024.07.002. Epub 2024 Jul 6.

Subregion-specific transcriptomic profiling of rat brain reveals sex-distinct gene expression impacted by adolescent stress

Kristen N Krolick  1 , Jingyi Cao  2 , Evelyn M Gulla  3 , Meeta Bhardwaj  4 , Samantha J Marshall  5 , Ethan Y Zhou  5 , Andor J Kiss  6 , Fouad Choueiry  7 , Jiangjiang Zhu  8 , Haifei Shi  9
Affiliations

Subregion-specific transcriptomic profiling of rat brain reveals sex-distinct gene expression impacted by adolescent stress

Kristen N Krolick et al. Neuroscience. .

Abstract

Stress during adolescence clearly impacts brain development and function. Sex differences in adolescent stress-induced or exacerbated emotional and metabolic vulnerabilities could be due to sex-distinct gene expression in hypothalamic, limbic, and prefrontal brain regions. However, adolescent stress-induced whole-genome expression changes in key subregions of these brain regions were unclear. In this study, female and male adolescent Sprague Dawley rats received one-hour restraint stress daily from postnatal day (PD) 32 to PD44. Corticosterone levels, body weights, food intake, body composition, and circulating adiposity and sex hormones were measured. On PD44, brain and blood samples were collected. Using RNA-sequencing, sex-specific differences in stress-induced differentially expressed (DE) genes were identified in subregions of the hypothalamus, limbic system, and prefrontal cortex. Canonical pathways reflected well-known sex-distinct maladies and diseases, substantiating the therapeutic potential of the DE genes found in the current study. Thus, we proposed specific sex distinct, adolescent stress-induced transcriptional changes found in the current study as examples of the molecular bases for sex differences witnessed in stress induced or exacerbated emotional and metabolic disorders. Future behavioral studies and single-cell studies are warranted to test the implications of the DE genes identified in this study in sex-distinct stress-induced susceptibilities.

Keywords: Amygdala; Chronic restraint stress; Hippocampus; Hypothalamus; Orbitofrontal cortex; Sex-specific differences.

PubMed Disclaimer

Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1.
Fig. 1.
The schematic of experimental design and brain regions. 1A. Schematic of experimental design. Female and male rats were monitored for food intake and body weights daily starting on PD28 till PD44, and weekly afterwards. Restraint stress or nonstress condition were performed during adolescence on PD32-PD44, for 13 consecutive days at random times during the light phase. During stress or nonstress, tail-blood plasma for corticosterone measurements was serially collected on the 1st day of stress (PD32) and 12th day of stress (PD43). Half of each group were euthanized for brain subregion RNA sequencing analysis one hour after stress on PD44 during adolescence, and the half of each group were kept alive until early adulthood on PD64. Plasma from PD44 and PD64 were used to measure hormones, including estradiol, testosterone, leptin, and insulin. Body composition was measured on PD31, PD43, and PD56. All female rats were monitored for their estrous cycles and were euthanized in the estrus. Created with BioRender.com. 1B. Schematic of brain subregion punches in brain atlas diagram. See methods for complete Bregma levels. Palkovits punch technique of 9 discrete brain regions: OFC (yellow), PVN (dark blue), ARC (red), VMH (green), CEA: (purple), and BLA (orange), CA1 (light blue), CA3 (pink), and DG (gold). Modified from Paxinos and Watson (2013).
Fig. 2.
Fig. 2.
Corticosterone levels and corresponding areas under the curves (AUC) of female and male nonstress and stress rats. 2A. Stress and nonstress female CORT level and AUC on the 1st day PD32. 2B. Stress and nonstress female CORT level and AUC on the 12th day PD43. 2C. Stress and nonstress male CORT level and AUC on the 1st day PD32. 2D. Stress and nonstress male CORT level and AUC on the 12th day PD43.AUC was calculated from 0- to 60-minute timepoints. Average ± SEM. * Indicates statistical significance between nonstress and stress groups within each sex (n = 12/group, P < 0.05).
Fig. 3.
Fig. 3.
Body weight, cumulative food intake, and body composition of female and male stress and nonstress rats. 3A. Body weight of stress and nonstress female rats. 3B. Cumulative food intake of stress and nonstress female rats. 3C. Body weight of stress and nonstress male rats. 3D. Cumulative food intake of stress and nonstress male rats. 3E. Body fat mass of stress and nonstress female rats. 3F. Body lean mass of stress and nonstress female rats. 3G. Body fat mass of stress and nonstress male rats. 3H. Body lean mass of stress and nonstress male rats. Average ± SEM. * Indicates statistical significance between nonstress and stress groups within each sex (P < 0.05). For all groups, on or before PD 44 n = 12/group, after PD 44 n = 6/group.
See this image and copyright information in PMC

Similar articles

See all similar articles

References

    1. Abdallah CG, Geha P, 2017. Chronic pain and chronic stress: two sides of the same coin? Chronic Stress (Thousand Oaks) 1. 10.1177/2470547017704763. - DOI - PMC - PubMed
    1. Admon R, Lubin G, Stern O, Rosenberg K, Sela L, Ben-Ami H, Hendler T, 2009. Human vulnerability to stress depends on amygdala's predisposition and hippocampal plasticity. PNAS 106 (33), 14120–14125. 10.1073/pnas.0903183106. - DOI - PMC - PubMed
    1. Albert PR, 2015. Why is depression more prevalent in women? J. Psychiatry Neurosci 40 (4), 219–221. 10.1503/jpn.150205. - DOI - PMC - PubMed
    1. Anacker C, Zunszain PA, Carvalho LA, Pariante CM, 2011. The glucocorticoid receptor: pivot of depression and of antidepressant treatment? Psychoneuroendocrinology 36 (3), 415–425. 10.1016/j.psyneuen.2010.03.007. - DOI - PMC - PubMed
    1. Anders S, Huber W, 2010. Differential expression analysis for sequence count data. Genome Biol. 11. 10.1186/gb-2010-11-10-r106. - DOI - PMC - PubMed