Phillip R. Zoladz

TL;DR: It is proposed that with the onset of strong emotionality, the hippocampus rapidly shifts from a “configural/cognitive map” mode to a ‘flashbulb memory’ mode, which underlies the long-lasting, but fragmented, nature of traumatic memories.

TL;DR: Evidence is provided that traumatic stress occurring in adulthood can induce CNS gene methylation, and the hypothesis that epigenetic marking of the Bdnf gene may underlie hippocampal dysfunction in response to traumatic stress is supported.

TL;DR: A thorough assessment of the literature indicates that interactions among myriad susceptibility factors, including social support, early life stress, sex, age, peri-and post-traumatic dissociation, cognitive appraisal of trauma, neuroendocrine abnormalities and gene polymorphisms, in conjunction with the inconsistent expression of the disorder across studies, confound attempts to characterize PTSD as a monolithic disorder as discussed by the authors.

TL;DR: An assessment of the literature indicates that interactions among myriad susceptibility factors, including social support, early life stress, sex, age, peri- and post-traumatic dissociation, cognitive appraisal of trauma, neuroendocrine abnormalities and gene polymorphisms, confounds attempts to characterize PTSD as a monolithic disorder.

TL;DR: Overall, it is found that an intense, ethologically relevant stressor produced a largely equivalent impairment of memory in male and female rats, and sex-independent corticosterone-memory correlations, which may provide insight into commonalities in how traumatic stress affects the brain and memory in men and women.