Empathy is perhaps the most human of all human traits, but relatively little is understood about how empathy works on a biochemical and neurological level.   In a recent paper by Pisansky et al. the authors examine the phenomenon of fear-contagion, an empathy-like response in mice, and whether oxytocin might play a role in how animals react to the stress of others.

Mice exhibit fear contagion as initial freezing behavior followed by escape behavior in response to the distress of another mouse.  In other words, watching a frightened mouse makes the observer mouse behave essentially as if it too has been frightened.  As with empathy in humans, females have a higher tendency to exhibit fear contagion overall as compared males under similar circumstances.   And in male mice, fear response was both more likely and stronger and when the observer mouse and the frightened mouse were well known to one another (littermates) as compared to strangers.   In humans, intranasal oxytocin is known to bolster emotional recognition and empathy.   Pisanskey et al. questioned whether oxytocin might exhibit similar effects on mice and whether fear contagion might be influenced by oxytocin.

Using male mice (because of their lower default levels of fear contagion response) the researchers administered a single intranasal dose of oxytocin 30 minutes prior to the fear response test.   To confirm that the intranasal oxytocin treatment was sufficient to raise cerebral oxytocin levels, some mice were sacrificed at the 30 minute time point and CSF and brain tissue assayed for oxytocin (Oxytocin EIA Kit, K048-H).  CSF levels of oxytocin were found to be elevated after intranasal treatment, however brain tissue levels were not detectable by EIA.

The oxytocin treated male mice showed no difference in the level of fear contagion between littermates, but did significantly increase both the frequency and intensity of the fear contagion response between mice that were not known to one another.

Decreasing oxytocin signaling via a chemical antagonist at the oxytocin receptor decreased fear contagion behaviors further substantiating to role of oxytocin in this response.   In order to insure that oxytocin was affecting the socially transmitted or contagious fear response rather than simply altering response to fear overall, the oxytocin treatments were repeated but this time on mice directly exposed to the fear stimulating foot shock test.   No significant changes were observed in the primary fear responses supporting the hypothesis that oxytocin’s role is specific to the social transfer of fear from one mouse to another, rather than the experience of fear itself.   Vocalizations of the demonstrator, or frightened mice, were also determined to play a key role in the transmission of fear to the observer mouse; with the familiar pairs again showing higher response than the mice that were strangers.

Overall it is clear that oxytocin signaling plays a significant role in fear contagion in mice, as well as important roles in various forms of emotional recognition and transmission in humans.   As we learn more about this important hormone it may provide insight into how to help people who struggle with empathy and appropriate emotional response.

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