Abstract
Alcohol is a traditional social-bonding reinforcer; however, the neural mechanism underlying ethanol-driven social behaviors remains elusive. Here, we report that ethanol facilitates observational fear response. Observer mice exhibited stronger defensive immobility while observing cagemates that received repetitive foot shocks if the observer mice had experienced a brief priming foot shock. This enhancement was associated with an observation-induced recruitment of subsets of anterior cingulate cortex (ACC) neurons in the observer mouse that were responsive to its own pain. The vicariously activated ACC neurons projected their axons preferentially to the basolateral amygdala. Ethanol shifted the ACC neuronal balance toward inhibition, facilitated the preferential ACC neuronal recruitment during observation, and enhanced observational fear response, independent of an oxytocin signaling pathway. Furthermore, ethanol enhanced socially evoked fear response in autism model mice.
Highlights
Alcohol is a traditional social-bonding reinforcer; the neural mechanism underlying ethanol-driven social behaviors remains elusive
We discovered that neuronal representations of experienced and observed pain overlapped at the single-cell level and were bidirectionally manipulable by administration of ethanol or an oxytocin receptor antagonist, which induced a corresponding change in defensive immobility during fear observation
We observed that the degrees of defensive immobility during observation were positively correlated with the overlap scores of anterior cingulate cortex (ACC) neurons but not with the absolute numbers of activated neurons, consistent with a report showing that the strength of fear memory is not coded by the overall size of memory trace in the lateral amygdala[40]
Summary
Alcohol is a traditional social-bonding reinforcer; the neural mechanism underlying ethanol-driven social behaviors remains elusive. Human brain imaging studies suggest that vicarious experience of others’ pain involves shared representation of experienced and observed pain[9,10]. This notion raises a possibility that this overlapping neural representation may underlie the experiencedependent facilitation of empathy. Affective empathy is modeled using the fear observational system, in which an animal (observer) exhibits behavioral defensive immobility when it observes the distress of a conspecific (demonstrator) receiving electrical shocks[15,16] In this fear transmission system, the anterior cingulate cortex (ACC), a pain-relevant brain region, is critical for experiencing vicarious pain[15], consistent with human imaging studies[9,10].
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