AI Article Synopsis
- There are notable sex differences in vulnerability to fear-related anxiety disorders, with females being twice as likely to develop PTSD compared to males.
- Female mice show resistance to fear extinction and demonstrate increased DNA methylation of the Bdnf gene, leading to decreased BDNF mRNA expression in the medial prefrontal cortex.
- Activating BDNF signaling through a specific agonist can prevent the return of fear in female mice after extinction training, suggesting a potential new treatment strategy for fear-related anxiety disorders.
Article Abstract
There are significant sex differences in vulnerability to develop fear-related anxiety disorders. Females exhibit twice the rate of post-traumatic stress disorder (PTSD) as males and sex differences have been observed in fear extinction learning in both humans and rodents, with a failure to inhibit fear emerging as a precipitating factor in the development of PTSD. Here we report that female mice are resistant to fear extinction, and exhibit increased DNA methylation of Bdnf exon IV and a concomitant decrease in mRNA expression within the medial prefrontal cortex. Activation of BDNF signaling by the trkB agonist 7,8-dihydroxyflavone blocks the return of fear in female mice after extinction training, and thus represents a novel approach to treating fear-related anxiety disorders that are characterized by a resistance to extinction and increased propensity for renewal.
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| http://dx.doi.org/10.1101/lm.029520.112 | DOI Listing |
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