Homologizing human emotions

Lawrence, Andrew David; Calder, Amanda Jane

doi:10.1093/acprof:oso/9780198528975.003.0002

Cited by 32 publications

(15 citation statements)

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“…This selective association with anger expression recognition is congruent with those theories which sustain that different neural systems exist that specialize, at least in part, in recognizing different types of emotional expressions (Kumfor et al 2013). These systems would be related with the evolutionary history (Lawrence and Calder 2004). The processing of aggression signals, that is extremely relevant for survival, has been related with the dopaminergic system in various species (Lawrence et al 2002) and is modulated by other relevant genetic and epigenetic biomarkers for social behavior like those related to oxytocin (Puglia et al 2015).…”

Section: Discussionsupporting

confidence: 84%

The ANKK1/DRD2 locus is a genomic substrate for affective priming and recognition of angry faces

et al. 2015

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IntroductionAnkyrin repeat and kinase domain containing I (ANKK1) and dopamine D2 receptor (DRD2) genes have been associated with psychopathic traits in clinical samples. On the other hand, individuals high in psychopathy show reduced affective priming and deficits in facial expression recognition. We have hypothesized that these emotion‐related cognitive phenomena are associated with Taq IA (rs18000497) SNP (single nucleotide polymorphism) of the ANKK1 gene and with C957T (rs6277) SNP of the DRD2 gene.MethodsWe performed a genetic association analysis in 94 self‐reported Caucasian healthy volunteers. The participants completed 144 trials of an affective priming task, in which primes and targets were emotional words. They also had to recognize 64 facial expressions of happiness, sadness, anger, and fear in an expression recognition task. Regarding the genetic analyses, Taq IA and C957T SNPs were genotyped.ResultsWe found that the C957T SNP TT genotype was associated with a stronger priming effect and a better recognition of angry expressions. No associations were found for the Taq IA SNP. In addition, in silico analysis demonstrated that C957T SNP is a marker of a regulatory sequence at the 5′ UTR of ANKK1 gene, thus suggesting the involvement of the whole ANKK1/DRD2 locus in cognitive–emotional processing.ConclusionsThese results suggest that affective priming and recognition of angry facial expressions are endophenotypes that lie on the pathway between the ANKK1/DRD2 locus and some deviant phenotypes.

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Section: Discussionsupporting

confidence: 84%

The ANKK1/DRD2 locus is a genomic substrate for affective priming and recognition of angry faces

et al. 2015

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“…A viewer may draw on information from an amygdala-based fear simulation to reconstruct and identify the expresser's emotional state (Goldman & Sripada, 2005;Lawrence & Calder, 2004). This explanation specifies that reduced fear responding will be associated with impaired fearful expression recognition.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Deficits in facial affect recognition among antisocial populations: A meta-analysis

Marsh

Blair

2008

Neuroscience & Biobehavioral Reviews

743

618

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Individuals with disorders marked by antisocial behavior frequently show deficits in recognizing displays of facial affect. Antisociality may be associated with specific deficits in identifying fearful expressions, which would implicate dysfunction in neural structures that subserve fearful expression processing. A meta-analysis of 20 studies was conducted to assess: (a) if antisocial populations show any consistent deficits in recognizing six emotional expressions; (b) beyond any generalized impairment, whether specific fear recognition deficits are apparent; and (c) if deficits in fear recognition are a function of task difficulty. Results show a robust link between antisocial behavior and specific deficits in recognizing fearful expressions. This impairment cannot be attributed solely to task difficulty. These results suggest dysfunction among antisocial individuals in specified neural substrates, namely the amygdala, involved in processing fearful facial affect. KeywordsFacial affect; fearful expression; antisocial; amygdala; psychopathy; emotion; meta-analysis Processing facial affect is crucial for socialization and normal social interaction (Corden et al. 2006;Fridlund, 1991). Aggression and other maladaptive antisocial behaviors may result from failure to be appropriately guided by the social cues of others (Blair, 2003a;Montagne et al. 2005;Walker and Leister, 1994). Some have suggested that distress-related cues, particularly fearful expressions, play an important role in inhibiting antisocial behavior (Blair, 2001;Nichols, 2001;Price, 2004). Accordingly, many studies find impairments in processing distress-related cues among antisocial populations. Not all studies find this impairment, however. It is unclear whether these inconsistencies result from disparate methodologies, sample populations, or analytic techniques, or, alternately, from the absence of a strong relationship between fearful affect processing and antisociality. Better understanding of facial affect recognition deficits associated with antisociality would permit more precise hypotheses to be formulated regarding neurocognitive correlates of antisocial behavior. We thus conducted this meta-analysis to assess associations between antisociality and facial affect recognition deficits. We hypothesized that, beyond any general facial affect recognition deficits, antisocial individuals show specific deficits in processing fearful expressions. We also hypothesized that such deficits are not solely attributable to task difficulty.*Address correspondence to: Abigail Marsh, Ph.D., Mood and Anxiety Program, National Institute of Mental Health, 15K North Drive, MSC 2670, Bethesda, MD, 20892. Email: marsha@mail.nih.gov; Tel: (301) Fax: (301) 402−6353. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it ...

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“…5 Perhaps most notably, studies indicate that deficits in the production or experience of various emotions are highly correlated with an inability to recognize those emotions in others. These results suggest that one must experience fear, anger, or disgust in order to come to know that someone else is afraid, angry, or disgusted, respectively (Adolphs et al 1994;Sprengelmeyer et al 1999;Lawrence and Calder 2004;Lawrence et al 2002;Calder et al 2000) This hypothesis receives further support from studies indicating that similar brain regions are activated during the experience of an emotion and the recognition of that emotion in another (Hein & Singer 2008;Jabbi et al 2007;Wicker et al 2003;Phillips et al 1997Phillips et al , 1998. Similar results are provided by research into mirror neurons.…”

Section: Empathy and Its Role In Moralitymentioning

confidence: 58%

Empathy and Its Role in Morality

Masto¹

2015

The Southern J of Philosophy

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In this paper, I will argue, contra Prinz, that empathy is a crucial component of our moral lives. In particular, I argue that empathy is sometimes epistemologically necessary for identifying the right action; that empathy is sometimes psychologically necessary for motivating the agent to perform the right action; and that empathy is sometimes necessary for the agent to be most morally praiseworthy for an action.

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Homologizing human emotions

Cited by 32 publications

References 0 publications

The ANKK1/DRD2 locus is a genomic substrate for affective priming and recognition of angry faces

The ANKK1/DRD2 locus is a genomic substrate for affective priming and recognition of angry faces

Deficits in facial affect recognition among antisocial populations: A meta-analysis

Empathy and Its Role in Morality

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