The four conditions of 156 trials (neutral or fear expression, central or peripheral position) were randomly presented.
Retention tests revealed opposite effects on fear expression despite identical behavioral treatments: intra-hippocampal DCS inhibited fear expression while intra-amygdala DCS potentiated fear expression.
For this reason, a different sentiment, joy, was extracted to compare changes of the fear expression at the same time.
Moreover, differences in hippocampal FGF2 expression were evident between high and low fear rats even three months following the tests for conditioned fear expression.
Together, these results suggest that individual differences in conditioned fear expression may be mediated partly by enduring differences in hippocampal functioning.
One potential biological target for reducing fear expression in PTSD is the hypothalamic-pituitary-adrenal (HPA) axis, which is dysregulated in PTSD.
We conducted a double-blind, placebo-controlled trial to test our hypothesis that dexamethasone administration and the concomitant suppression of HPA axis hyperactivity would attenuate fear expression and enhance fear extinction in individuals with PTSD.
Rodent studies of individual differences in fear expression following Pavlovian fear conditioning are thought to provide useful means by which to examine the factors associated with vulnerability and resilience to anxiety and trauma- and stressor-related disorders in humans.
This increased fear load associated with PTSD can be a barrier to effective therapy thus indicating the need for new treatments to reduce fear expression in people with PTSD.
Although we were mainly interested in capturing changes in fear expression from the tweet text, it is important to understand whether the changes reflect meaningful changes in sentiments, or just reflect changes in the tweet volumes.
Maybe [the] RDoC is going to be very helpful and we are going to be able to say: "You have [this or that degree of] a deficit in the negative affect domain in fear expression".
