Neurobiologische Mechanismen des Wiederauftreten von Furcht im sozialen Kontext
Zusammenfassung der Projektergebnisse
This project aimed to investigate the social control of fear conditioned responses. The studies focused on the interaction between direct and social learning, i.e. how we learn from direct, aversive experiences and through aversive experiences as observed in another individual. Three studies revealed that conditioned fear responses that are acquired through direct aversive experiences can return after observation of aversive events in others (“Observational Reinstatement”). Interestingly, conditioned fear responses returned in psychophysiological arousal (skin-conductance responses), but not in defensive responses as measured as fear potentiated startle. In order to follow up on these unexpected results, the initially planned study to examine neural mechanisms of observational reinstatement was replaced by a study to compare the neural processes involved in direct and observational learning from aversive events (using direct and observational fear conditioning). First, the methodological considerations emerging from previous experiments employing observational fear conditioning were systematically reviewed. Then, a fMRI study revealed that observational and direct fear conditioning involves a common neural network, but engages a different information flow (inter-regional connectivity examined by dynamic causal modeling). The following study explored if observational fear conditioning relies on similar neurotransmitter pathways that have been implied by previous studies on direct fear conditioning, i.e. endogenous opioids. This pharmacological fMRI study (using an opioid receptor antagonist Naltrexone as compared to Placebo) revealed that observation of aversive events in others is coded by endogenous opioid transmission in a similar way as during direct experience of these events. Blockade of opioid transmission enhanced neural coding of observational fear conditioning in the amygdala, periaqueductal gray and midline thalamus and predicted expression of fear 72 hours later. In sum these results advance the knowledge how direct and social learning from aversive events interact. Additionally, they provide the first neuropharmacological model of social threat learning in humans. These insights might help to undertstand the etiology and advance the treatment of socially acquired fear in common psychiatric conditions, such as anxiety related disorders.
