Abstract

The neural basis of empathy and prosociality has received much interest over the past decades. Neuroimaging studies localized a network of brain regions with activity that correlates with empathy. Here, we review how the emergence of rodent and nonhuman primate models of empathy-related phenomena supplements human lesion and neuromodulationstudies providing evidence that activity in several nodes is necessary for these phenomena to occur. We review proof that (i) affective states triggered by the emotions of others, (ii) motivations to act in ways that benefit others, and (iii) emotion recognitioncan be altered by perturbing brain activity in many nodes identified by human neuroimaging, with strongest evidence for the cingulate and the amygdala. We also include evidence that manipulations of the oxytocin system and analgesics can have such effects, the latter providing causal evidence for the recruitment of an individual's own nociceptive system to feel with the pain of others.

Highlights

  • People disagree on what empathy exactly is, most agree it includes feeling what another person feels

  • Emotion recognition In mice, inhibiting oxytocinergic paraventricular nucleus neurons projecting to the central amygdala (CeA), but not nucleus accumbens (NAc), mPFC, and hippocampus, impaired the discrimination of fear and relief states without effects on sociability [76*]; and infusion of oxytocin receptor antagonist (OTA) in the insula reduces the tendency of rats to interact with stressed juvenile over stressed adults [40]

  • Infusion of Conclusions While functional magnetic resonance imaging flagged regions with activity correlating with empathy (Figure 1), neuromodulation studies (Figure 2) reveal how far we have come in showing that many of these nodes are necessary for emotional contagion, vicarious learning, and some motivations to engage in behaviors that improve outcomes for others

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Summary

Introduction

People disagree on what empathy exactly is, most agree it includes feeling what another person feels. An important role in emotional contagion has been assigned to a subset of interneurons in the anterior cingulate cortex (ACC), somatostatin-expressing (SSTþ) interneurons, whose optogenetic silencing increases and activation decreases vicarious freezing [16**] Another group of studies examined the reaction of rats to witnessing a demonstrator hear a previously shock-associated CSþ. Emotion recognition In mice, inhibiting oxytocinergic paraventricular nucleus neurons projecting to the CeA, but not NAc, mPFC, and hippocampus, impaired the discrimination of fear and relief states without effects on sociability [76*]; and infusion of OTA in the insula reduces the tendency of rats to interact with stressed juvenile over stressed adults [40].

Conclusions
Yamamoto S
51. Adolphs R
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