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Epigenetic modification of hippocampal Bdnf DNA in adult rats in an animal model of post-traumatic stress disorder
Open accessAbstract
Epigenetic alterations of the brain-derived neurotrophic factor (Bdnf) gene have been linked with memory, stress, and neuropsychiatric disorders. Here we examined whether there was a link between an established rat model of post-traumatic stress disorder (PTSD) and BdnfDNA methylation. Adult male Sprague-Dawley rats were given psychosocial stress composed of two acute cat exposures in conjunction with 31 days of daily social instability. These manipulations have been shown previously to produce physiological and behavioral sequelae in rats that are comparable to symptoms observed in traumatized people with PTSD. We then assessed BdnfDNA methylation patterns (at exon IV) and gene expression. We have found here that the psychosocial stress regimen significantly increased BdnfDNA methylation in the dorsal hippocampus, with the most robust hypermethylation detected in the dorsal CA1 subregion. Conversely, the psychosocial stress regimen significantly decreased methylation in the ventral hippocampus (CA3). No changes in BdnfDNA methylation were detected in the medial prefrontal cortex or basolateral amygdala. In addition, there were decreased levels of BdnfmRNA in both the dorsal and ventral CA1. These results provide evidence that traumatic stress occurring in adulthood can induce CNS gene methylation, and specifically, support the hypothesis that epigenetic marking of the Bdnfgene may underlie hippocampal dysfunction in response to traumatic stress. Furthermore, this work provides support for the speculative notion that altered hippocampal BdnfDNA methylation is a cellular mechanism underlying the persistent cognitive deficits which are prominent features of the pathophysiology of PTSD.
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Metadata
- Authors
- Roth, T. L., Zoladz, P. R., Sweatt, J. D., & Diamond, D. M.
- Venue
- Journal of Psychiatric Research
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 45
- Issue
- 7
- Pages
- 919-926
- ISSN
- 0022-3956 (ISSN-L)
- OpenAlex
- W2160621075
- Cited by
- 323
- References
- 26
- FWCI
- 39.32
- Type
- journal article
- Language
- en
- Open access
- green
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