We found matching results for the static S1 faces: fearfulness of static S1 faces (28%, 45%, or 63%) strongly enhanced fear perception of S2 faces, reflected by a significant main effect of static S1 fearfulness, F2,40 = 13.93, MSE = 0.09, P < 0.0001.
The enhanced fear response of HAB mice was attenuated by treatment with either the α2,3,5-subunit selective benzodiazepine partial agonist L-838,417, corticosterone or the selective neurokinin-1 receptor antagonist L-822,429.
Some revealed a general increase of fear reactions, both to the fear (CS+) and the safety stimulus (CS−), whereas other studies discovered a differential return of fear with enhanced fear responses to the CS+ only.
Neutralization of FGF2 revealed that astrocyte-secreted FGF2 mediated stress-hormone-induced NPC proliferation. 2 weeks, but not 2 days, after acute stress, rats also showed enhanced fear extinction memory coincident with enhanced activation of newborn neurons.
The mice lacking the gene showed striking behavioral differences from normal, healthy mice as they exhibited classic signs of depression such as behavioral despair and enhanced fear memory.
An important aim currently in the fear and anxiety field is the identification of the HDAC isoform(s) contributing to or mediating enhanced fear extinction.
An increased fear response may be due to enhanced fear memory or enhanced anxiety-like behavior, a decreased fear response may be due to impaired fear memory or less anxiety, while a minor change or non-change in fear response, such as in 36 trials-triggered fear response in current study, may be due to a mixture of impaired fear memory and enhanced anxiety-like behavior.
Finally, enhanced fear-relevant schemas in the context of external stimuli have been proposed to contribute to the formation of excessive anxiety (Teachman et al. 2001).
