Oxytocin in the anterior cingulate cortex is involved in helping behaviour

Yamagishi, Atsuhito; Lee, Joungmin; Sato, Nobuya

doi:10.1016/j.bbr.2020.112790

Cited by 40 publications

(36 citation statements)

References 64 publications

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“…27,28 Therefore, we conducted an autoradiography study using radiolabeled OVT ligand on coronal sections of WT and CD brains (Figure 3A). As well as measuring regions relevant to fear conditioning (BLA and LA; 51,52 LSN 31 ), we measured areas of where OT has been shown to affect sociability or memory (AON; 53 LSN; 54 ACC; 55,56 CA2/3; 57,58 Pir; 59 PVN 60 ; and CPu 25 )(Figure 3B), as hypersociability and cognitive impairments are characteristic of WS. We found no significant differences in OXTR binding between genotypes within regions of interest in CD and WT brains when corrected for multiple testing (Figure 3C, Supplemental Table 2).…”

Section: Resultsmentioning

confidence: 99%

Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model

Nygaard

Swift

Glick

et al. 2021

Preprint

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Williams Syndrome is caused by a deletion of 26-28 genes on chromosome 7q11.23. Patients with this disorder have distinct behavioral phenotypes including learning deficits, anxiety, increased phobias, and hypersociability. Some studies also suggest elevated blood oxytocin and altered oxytocin receptor expression, and this oxytocin dysregulation is hypothesized to be involved in the underlying mechanisms driving a subset of these phenotypes. A 'Complete Deletion' mouse, modeling the hemizygous critical region deletion in Williams Syndrome, recapitulates many of the phenotypes present in humans. These Complete Deletion mice also exhibited impaired fear responses in the conditioned fear task. Here, we address whether oxytocin dysregulation is responsible for this impaired associative fear memory response. We show direct delivery of an oxytocin receptor antagonist to the central nervous system did not rescue the attenuated contextual or cued fear memory responses in Complete Deletion mice. Thus, increased oxytocin signaling is not acutely responsible for this phenotype. We also evaluated oxytocin receptor and serotonin transporter availability in regions related to fear learning, memory, and sociability using autoradiography in wild type and Complete Deletion mice. While we identified trends in lowered oxytocin receptor expression in the lateral septal nucleus, and trends towards lowered serotonin transporter availability in the striatum and orbitofrontal cortex, we found no significant differences after correction. Together, these data suggest the fear conditioning anomalies in the Williams Syndrome mouse model are independent of any alterations in the oxytocinergic system caused by deletion of the Williams locus.

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Section: Resultsmentioning

confidence: 99%

Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model

Nygaard

Swift

Glick

et al. 2021

Preprint

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“…Furthermore, both in zebrafish and in rodents oxytocin also regulates emotion recognition [23,26], which is the cognitive basis for emotion contagion. Therefore, it is plausible that oxytocin has been recruited early in the evolution of nonapeptides to regulate ancestral empathic behaviors in group living species, and that it has been evolutionary co-opted to regulate more complex empathic behaviors, such as consolation and helping [24,[27][28][29][30], in species with more complex cognitive abilities. From a translational research perspective our results provide content and construct validity to a phylogenetically distant model of emotional contagion.…”

Section: Main Textmentioning

confidence: 99%

Oxytocin regulation of social transmission of fear in zebrafish reveals its evolutionary conserved role in emotional contagion

Akinrinade

Kareklas

Gliksberg

et al. 2021

Preprint

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Emotional contagion is the most ancestral form of empathy that relies on simple perception-action mechanisms, on top of which more complex forms of empathic behaviors, such as consolation and helping, have evolved. Here we tested to what extent the proximate mechanisms of emotional contagion are evolutionary conserved by assessing the role of oxytocin, known to regulate empathic behaviors in mammals, in social fear contagion in zebrafish, which represents an evolutionary divergent line to that of tetrapods, within vertebrates. Using mutants for the ligand of the fish oxytocin nonapeptide and both of its receptors in zebrafish we showed that oxytocin is necessary for observer zebrafish to copy the distressed behavior of conspecific demonstrators. Exogeneous administration of oxytocin to the ligand mutant rescued the ability of observers to express social fear transmission, indicating that oxytocin is not only necessary but also sufficient for emotional contagion. The brain regions in the ventral telencephalon that are associated with emotional contagion in zebrafish are homologous to those known to be involved in the same process in rodents (e.g. striatum, lateral septum), and receive direct projections from oxytocinergic neurons located in the preoptic area. Finally, we ruled out the hypothesis that social transmission of fear in zebrafish merely relies on behavior contagion by motor imitation, and we showed that it rather relies on emotion discrimination. Together our results support an evolutionary conserved role for oxytocin as a key regulator of basic empathic behaviors across vertebrates.

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“…The existence of empathy has been suggested in a variety of species, including non-human primates (Campbell and de Waal, 2011; Koski and Sterck, 2010; Pruetz, 2011), dogs (Palagi et al, 2015), birds (Gallup et al, 2015), and even rodents (Bartal et al, 2011; Bartal et al, 2016; Sato et al, 2015). Several studies have examined empathy in rodents using behavioral indicators, such as vicarious learning of fear (Atsak et al, 2011; Pisansky et al, 2017) and helping behavior like releasing others from a distressed situation (Bartal et al, 2011; Bartal et al, 2016; Sato et al, 2015; Yamagishi et al, 2019; Yamagishi et al, 2020). However, understanding of empathy in rodents is still inadequate.…”

Section: Introductionmentioning

confidence: 99%

“…Helping behavior has been observed in animals that are considered to be highly intelligent, such as chimpanzees (Pruetz, 2011; Yamamoto et al, 2012), elephants (Schulte, 2000), and dolphins (Kuczaj et al, 2015). Recent studies suggest that rats also demonstrate helping behavior toward distressed conspecifics, such as in a narrow tube (Bartal et al, 2011; Bartal et al, 2016) and in water (Sato et al, 2015; Yamagishi et al, 2019; Yamagishi et al, 2020). Detecting others’ distress is a prerequisite for helping behavior (Cronin, 2012; Decety et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

“…Several studies have reported that oxytocin and oxytocin receptors in rodents affect sociality, including affiliative behavior, social cognition, and empathic response (Bartz et al, 2010; Marlin and Froemke, 2017; Rogers-Carter et al, 2018; Ross and Young, 2009; Winslow and Insel, 2002; Young and Barrett, 2015). The role of oxytocin in helping behavior is largely unexamined except in studies that examined the effect of oxytocin administration and of blocking of oxytocin receptors in rats (Yamagishi et al, 2020; Yamagishi et al, 2019). In this study, we examined the effects of oxytocin on helping behavior using oxytocin receptor knockout (OXTrKO) voles.…”

Section: Introductionmentioning

confidence: 99%

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Helping Behavior in Prairie Voles: A Model of Empathy and the Importance of Oxytocin

Kitano

Yamagishi

Horie

et al. 2020

Preprint

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Accumulated evidence across animals suggests that helping behavior is triggered by empathy. We examined whether prairie voles, one of the more highly social animals, help conspecifics who are soaked in water by opening a door to a safe area. Door-opening latency decreased as task sessions progressed, suggesting that prairie voles learn helping behavior. In addition, when the conspecific was not soaked in water, the latency of the door-opening did not decrease, suggesting that the distress of the conspecific is necessary for the learning of the door-opening. Thus, the door-opening behavior in prairie voles can be considered a helping behavior that is motivated by empathy for the distress of conspecifics. We also examined the helping behavior in prairie voles in which oxytocin receptors were genetically knocked out. Oxytocin receptor knockout voles demonstrated impaired learning of the door-opening. This suggests that oxytocin is important for the emergence of helping behavior.

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Oxytocin in the anterior cingulate cortex is involved in helping behaviour

Cited by 40 publications

References 64 publications

Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model

Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model

Oxytocin regulation of social transmission of fear in zebrafish reveals its evolutionary conserved role in emotional contagion

Helping Behavior in Prairie Voles: A Model of Empathy and the Importance of Oxytocin

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