WHAT HAPPENS AFTER FEAR? CENTRAL AMYGDALA ENKEPHALIN CELLS MEDIATE RECOVERY FROM AVERSIVE EXPERIENCES

Aversive experience and recuperation from it can be seen as interlinked processes which collectively define fear and anxiety inducing encounters. Despite this fact, fear has been thought to decay passively, merely due to the passage of time. We propose that returning to well-being is realized through an active motivational state comprising distinct neural signatures of information processing and observable behavioral outputs.
We found that time spent in a familiar environment after an aversive experience can alleviate its impact. In order to understand whether recuperation systems have any behavioral outputs, we observed mice after different aversive events and in different recuperative environments. Using unsupervised behavioral extraction methods and manual scoring, we discovered that mice indeed engages in self-attendance behaviors when the need for recuperation is high and the environment is feasible for recuperation.
We hypothesized that central amygdala enkephalin expressing cells (CeA-ENK) function as detectors for deviations from emotional normalcy to mobilize recuperation. Single-cell in vivo calcium imaging showed distinct CeA-ENK network trajectories in good and bad recuperators. In all mice, the distance between the state of the network during stress and homecage periods was large. In bad recuperators, this distance remained elevated towards the end of the stress; while in good recuperators, it decreased, suggesting that the network detects and regulates a return to normalcy. Consistent with the idea that coding in CeA-ENK mobilizes recuperation, CeA-ENK inhibition resulted in reduced recuperation, leading to higher levels of short term stress effects, and increased threat learning following traumatic events.