In addition, intranasal oxytocin also dampened the central fear response by lowering amygdala activity [ 44- 46] and potentially enhancing fear regulation by increasing top-down control of the prefrontal cortex over the amygdala [ 47].
However, as non-histone proteins are also acetylated by HDAC inhibitors [ 50], it is possible that direct acetylation of non-histone proteins also contributes to enhancing fear extinction memories.
In rats, tiny injections of norepinephrine into the amygdala, a region of the brain that encodes fear, can enhance fear conditioning.
Opiates also inhibit the production of a chemical messenger called norepinephrine, which is thought to enhance fear signals in the brain.
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.
These B6 subjects also exhibited enhanced fear learning (trials 7-10) relatove to BALB subjects (orthogonal contrast, P<0.001).
Using an experimental paradigm of learned fear in combination with mice selectively bred for either high or normal anxiety-related behaviour, these findings demonstrate an association between innate anxiety and enhanced fear expression.
For example, certain genetic variants are found to associate with the onset of anxiety [9], while no evidence indicates that those identified genetic variants are able to significantly enhance fear memory per se.
In other words, fear memory will be enhanced following an increase in the intensity of stress, while when the stress is strong to certain level, it would impair, but not enhance, fear memory, and consequently, lead to a less fear response in a subject.
