Abstract
Deficits in empathy have been proposed to constitute a hallmark of several psychiatric disturbances like conduct disorder, antisocial and narcissistic personality disorders. Limited sensitivity to punishment, shallow or deficient affect and reduced physiological reactivity to environmental stressors have been often reported to co-occur with limited empathy and contribute to the onset of antisocial phenotypes. Empathy in its simplest form (i.e. emotional contagion) is addressed in preclinical models through the evaluation of the social transmission of emotional states: mice exposed to a painful stimulus display a higher response if in the presence of a familiar individual experiencing a higher degree of discomfort, than in isolation. In the present study, we investigated whether a reduction of emotional contagion can be considered a predictor of reduced sociality, sensitivity to punishment and physiological stress reactivity. To this aim, we first evaluated emotional contagion in a group of Balb/cJ mice and then discretised their values in four quartiles. The upper (i.e. Emotional Contagion Prone, ECP) and the lower (i.e. Emotional Contagion Resistant, ECR) quartiles constituted the experimental groups. Our results indicate that mice in the lower quartile are characterized by reduced sociability, impaired memory of negative events and dampened hypothalamic-pituitary-adrenocortical reactivity to external stressors. Furthermore, in the absence of changes in oxytocin receptor density, we show that these mice exhibit elevated concentrations of oxytocin and vasopressin and reduced density of BDNF receptors in behaviourally-relevant brain areas. Thus, not only do present results translate to the preclinical investigation of psychiatric disturbances, but also they can contribute to the study of emotional contagion in terms of its adaptive significance.
Highlights
Empathy enables individuals to share the affective feeling of others, to anticipate their actions [1, 2] and it stimulates prosocial behaviour [3,4,5]
Here we addressed in particular conduct disorder (CD)
Control (CTRL) mice, tested in response to 0.2% formalin concentration, showed a large reduction in pain response compared to D mice (formalin dose: F(1,13) = 23.126; p < 0.01, Fig 3B, inset) and a single early peak in paw-licking, which steadily declined to near-zero levels immediately afterwards (repeated measures: F(5,20) = 3.049; p < 0.05)
Summary
Empathy enables individuals to share the affective feeling of others, to anticipate their actions [1, 2] and it stimulates prosocial behaviour [3,4,5]. Empathy is thought to have evolutionary precursors that allow animals to share emotional states even without being able to identify the source or to comprehend the causality of the emotion aroused in the other. This particular phenomenon was originally described in social animals by ethologists, who called it “Stimmungsubertragung” [9], translatable as “emotional contagion” or “mood induction” [1]. The construct of empathy is amenable to being addressed within the evolutionary adaptive framework offered by the Tinbergen four whys [13]: with respect to evolutionary adaptive considerations, the ability to empathize affects an individual’s behaviour toward others and the quality of social relationships, influencing individual fitness [14]; from an ontogenetic perspective, empathy is an important part of social development and its maturation cooccurs with emotional and cognitive processes; with respect to phylogeny, different levels of empathy have been identified in several taxa, ranging from rodents to elephants and chimpanzees [15]; the proximate causations and some of the fundamental biological mechanisms governing empathy across species have been identified [8]
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