| Summary: | Noor Shakfeh (1), Natalie Meylan (2), Robert Adamec (3), Ronald F. Mervis (2, 4) (1) The Honors College, USF, Tampa, FL; (2) Neurostructural Research Labs, Tampa, FL.; (3) Dept of Psychology, Memorial University, St. John’s, Newfoundland, Canada, (4) Center of Excellence for Aging and Brain Repair, Dept of Neurosurgery and Brain Repair, USF College of Medicine, Tampa, FL. Post-Traumatic Stress Disorder (PTSD) is an anxiety response to severe stress. There are individual differences in vulnerability. Not all individuals exposed to the same stressor show PTSD. The purpose of this study was to ascertain the relationship between anxiety levels and hippocampal brain circuitry: spine density on granule cells of the dentate gyrus. Predator stress (exposure to a cat) is an intense stressor. The response to the predator stress is also contingent upon whether the subject’s innate level of anxiety is low (e.g, well adapted) or high (e.g., mal-adapted). In a rat, this anxiety can be determined by an elevated plus maze. There were 4 groups of adult rats. Rats categorized as “less anxious” were either non-stressed (controls) or predator stressed; and, “high anxious” rats were also either non-stressed or predator stressed. Fixed brains were Golgi stained and from coded slides dendritic spine density was assessed. Spine density in high anxiety rats had significantly lower spine densities. Regardless of whether the rats were stressed or non-stressed, high anxiety rats had 10-13% fewer dendritic spines on their granule cells compared to the low anxiety rats. Thus hippocampal circuitry in the high anxiety rats is significantly altered from the low anxiety group.
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