Passive and Motivated Perception of Emotional Faces: Qualitative and Quantitative Changes in the Face Processing Network

Emotionally expressive faces are processed by a distributed network of interacting sub-cortical and cortical brain regions. The components of this network have been identified and described in large part by the stimulus properties to which they are sensitive, but as face processing research matures interest has broadened to also probe dynamic interactions between these regions and top-down influences such as task demand and context. While some research has tested the robustness of affective face processing by restricting available attentional resources, it is not known whether face network processing can be augmented by increased motivation to attend to affective face stimuli. Short videos of people expressing emotions were presented to healthy participants during functional magnetic resonance imaging. Motivation to attend to the videos was manipulated by providing an incentive for improved recall performance. During the motivated condition, there was greater coherence among nodes of the face processing network, more widespread correlation between signal intensity and performance, and selective signal increases in a task-relevant subset of face processing regions, including the posterior superior temporal sulcus and right amygdala. In addition, an unexpected task-related laterality effect was seen in the amygdala. These findings provide strong evidence that motivation augmentsco-activity among nodes of the face processing network and the impact of neural activity on performance. These within-subject effects highlight the necessity to consider motivation when interpreting neural function in special populations, and to further explore the effect of task demands on face processing in healthy brains

Neural Responses to Truth Telling and Risk Propensity under Asymmetric Information

This research was supported by the Laureate Institute for Brain Research and the William K. Warren Foundation. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.Trust is multi-dimensional because it can be characterized by subjective trust, trust antecedent, and behavioral trust. Previous research has investigated functional brain responses to subjective trust (e.g., a judgment of trustworthiness) or behavioral trust (e.g., decisions to trust) in perfect information, where all relevant information is available to all participants. In contrast, we conducted a novel examination of the patterns of functional brain activity to a trust antecedent, specifically truth telling, in asymmetric information, where one individual has more information than others, with the effect of varying risk propensity. We used functional magnetic resonance imaging (fMRI) and recruited 13 adults, who played the Communication Game, where they served as the “Sender” and chose either truth telling (true advice) or lie telling (false advice) regarding the best payment allocation for their partner. Our behavioral results revealed that subjects with recreational high risk tended to choose true advice. Moreover, fMRI results yielded that the choices of true advice were associated with increased cortical activation in the anterior rostral medial and frontopolar prefrontal cortices, middle frontal cortex, temporoparietal junction, and precuneus. Furthermore, when we specifically evaluated a role of the bilateral amygdala as the region of interest (ROI), decreased amygdala response was associated with high risk propensity, regardless of truth telling or lying. In conclusion, our results have implications for how differential functions of the cortical areas may contribute to the neural processing of truth telling.Yeshttp://www.plosone.org/static/editorial#pee

BOLD response during visual perception of biological motion in obsessive-compulsive disorder

Although research has shown that deficits in various cognitive functions may underlie obsessive-compulsive disorder (OCD), studies have not yet clarified the specificity and etiology of perception processing, particularly the perception of biological motion that is correlated with social cognition. We used functional magnetic resonance imaging (fMRI) to investigate neural activity associated with the perception of biological motion in OCD patients. The subjects were 15 patients with OCD and 15 age- and IQ-matched healthy volunteers. All subjects participated in a biological motion task in which they performed a one-back task signaling a repeated stimulus with a key press in each block condition to obligate attention to both types of stimuli. The biological motion versus scrambled motion contrast revealed that both OCD patients and healthy controls exhibited increased activation of the superior and middle temporal gyrus, the regions implicated in processing of biological motion, which is consistent with previous studies. However, direct comparison between OCD subjects and healthy controls indicated that patients with OCD exhibited increased activation in the right superior and middle temporal gyrus and the left inferior temporal and fusiform gyrus, and reduced activation in the right postcentral gyrus (BA 40) compared to healthy subjects. OCD patients exhibited increased activation in the ventral visual system, including the inferior temporal and fusiform gyrus. We observed a differential pattern of activity between OCD patients and healthy controls, indicating that OCD patients have functional differences related to the perception of biological motion. The differential activation between OCD patients and healthy subjects might contribute to the pathophysiological understanding of obsessive compulsive disorder.Grisham JR, 2008, EUR ARCH PSY CLIN N, V258, P107, DOI 10.1007/s00406-007-0789-0Olley A, 2007, J AFFECT DISORDERS, V104, P15, DOI 10.1016/j.jad.2007.02.023Shin YW, 2007, HUM BRAIN MAPP, V28, P1128, DOI 10.1002/hbm.20338Saygin AP, 2007, BRAIN, V130, P2452, DOI 10.1093/brain/awm162Blake R, 2007, ANNU REV PSYCHOL, V58, P47, DOI 10.1146/annurev.psych.57.102904.190152KIM J, 2007, DEPRESS ANX IN PRESSCalvo-Merino B, 2006, CURR BIOL, V16, P1905, DOI 10.1016/j.cub.2006.07.065Inoue Y, 2006, EUR ARCH PSY CLIN N, V256, P326, DOI 10.1007/s00406-006-0608-zWIENER D, 2006, PSYCHIAT POL, V40, P205Choi JS, 2006, DEPRESS ANXIETY, V23, P290, DOI 10.1002/da.20171Heberlein AS, 2005, NEUROIMAGE, V28, P770, DOI 10.1016/j.neuroimage.2005.06.064Kim JJ, 2005, SCHIZOPHR RES, V77, P299, DOI 10.1016/j.schres.2005.04.006Szeszko PR, 2005, ARCH GEN PSYCHIAT, V62, P782Loula F, 2005, J EXP PSYCHOL HUMAN, V31, P210, DOI 10.1037/0096-1523.31.1.210Shin MS, 2004, NEUROPSYCHOLOGY, V18, P665, DOI 10.1037/0894-4105.18.4.665Buccino G, 2004, BRAIN LANG, V89, P370, DOI 10.1016/S0093-934X(03)00356-0Saxe R, 2004, NEUROPSYCHOLOGIA, V42, P1435, DOI 10.1016/j.neuropsychologia.2004.04.015Gallese V, 2003, PSYCHOPATHOLOGY, V36, P171, DOI 10.1159/000072786Chen Y, 2003, SCHIZOPHR RES, V61, P215, DOI 10.1016/S0920-9964(02)00222-0Wheeler ME, 2003, J NEUROSCI, V23, P3869Pinkham AE, 2003, AM J PSYCHIAT, V160, P815Kang DH, 2003, ACTA PSYCHIAT SCAND, V107, P291Giese MA, 2003, NAT REV NEUROSCI, V4, P179, DOI 10.1038/nrn1057Blake R, 2003, PSYCHOL SCI, V14, P151Grossman ED, 2002, NEURON, V35, P1167Gallese V, 2002, ATTENTION PERFORM, V19, P334Rizzolatti G, 2001, NAT REV NEUROSCI, V2, P661SAXENA S, 2001, SEMIN CLIN NEUROPSYC, V6, P82Grossman E, 2000, J COGNITIVE NEUROSCI, V12, P711Allison T, 2000, TRENDS COGN SCI, V4, P267Baron-Cohen S, 2000, NEUROSCI BIOBEHAV R, V24, P355Adolphs R, 1999, TRENDS COGN SCI, V3, P469Mataix-Cols D, 1999, AM J PSYCHIAT, V156, P1409Watanabe K, 1998, PERCEPTION, V27, P1041FIRST MB, 1997, STRUCTURED CLIN INTEGOODALE MA, 1997, HDB NEUROPSYCHOLOGY, P91Cottraux J, 1996, PSYCHIAT RES, V60, P101LUCEY JV, 1995, BRIT J PSYCHIAT, V167, P629BARBAS H, 1988, J COMP NEUROL, V276, P313AGGLETON JP, 1980, BRAIN RES, V190, P347JOHANSSO.G, 1973, PERCEPT PSYCHOPHYS, V14, P2011