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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Aurbach, Elyse L. Chaudhury, Sraboni Sharma, Vikram Turner, Cortney A. Blandino, Peter Akil, Huda Watson, Stanley J. |
| Description | Author Affiliation: Chaudhury S ( Molecular and Behavioral Neuroscience Institute and sraboni@umich.edu akil@umich.edu.); Aurbach EL ( Molecular and Behavioral Neuroscience Institute and.); Sharma V ( Molecular and Behavioral Neuroscience Institute and.); Blandino P ( Molecular and Behavioral Neuroscience Institute and.); Turner CA ( Molecular and Behavioral Neuroscience Institute and.); Watson SJ ( Molecular and Behavioral Neuroscience Institute andDepartment of Psychiatry, University of Michigan, Ann Arbor, MI 48109.); Akil H ( Molecular and Behavioral Neuroscience Institute andDepartment of Psychiatry, University of Michigan, Ann Arbor, MI 48109 sraboni@umich.edu akil@umich.edu.); |
| Abstract | Posttranslational modifications of histone tails in chromatin template can result from environmental experiences such as stress and substance abuse. However, the role of epigenetic modifications as potential predisposing factors in affective behavior is less well established. To address this question, we used our selectively bred lines of high responder (bHR) and low responder (bLR) rats that show profound and stable differences in affective responses, with bLRs being prone to anxiety- and depression-like behavior and bHRs prone to addictive behavior. We first asked whether these phenotypes are associated with basal differences in epigenetic profiles. Our results reveal broad between-group differences in basal levels of trimethylated histone protein H3 at lysine 9 (H3K9me3) in hippocampus (HC), amygdala, and nucleus accumbens. Moreover, levels of association of H3K9me3 at Glucocorticoid Receptor (GR) and Fibroblast growth Factor 2 (FGF2) promoters differ reciprocally between bHRs and bLRs in these regions, consistent with these genes' opposing levels of expression and roles in modulating anxiety behavior. Importantly, this basal epigenetic pattern is modifiable by FGF2, a factor that modulates anxiety behavior. Thus, early-life FGF2, which decreases anxiety, altered the levels of H3K9me3 and its binding at FGF2 and GR promoters of bLRs rendering them more similar to bHRs. Conversely, knockdown of HC FGF2 altered both anxiety behavior and levels of H3K9me3 in bHRs, rendering them more bLR-like. These findings implicate FGF2 as a modifier of epigenetic mechanisms associated with emotional responsiveness, and point to H3K9me3 as a key player in the regulation of affective vulnerability. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 32 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-08-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Physiology Behavior, Animal Emotions Epigenesis, Genetic Fibroblast Growth Factor 2 Genetics Histones Chemistry Metabolism Animals Chromatin Assembly And Disassembly DNA Methylation Deficiency Gene Knockdown Techniques Hippocampus Promoter Regions, Genetic Receptors, Glucocorticoid Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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