Neuronal Correlates of Empathy: A Systematic Review of Event-Related Potentials Studies in Perceptual Tasks.

Empathy is a crucial component to infer and understand others' emotions. However, a synthesis of studies regarding empathy and its neuronal correlates in perceptual tasks using event-related potentials (ERPs) has yet to occur. The current systematic review aimed to provide that overview. Upon bibliographic research, 30 studies featuring empathy assessments and at least one perceptual task measuring ERP components in healthy participants were included. Four main focus categories were identified, as follows: Affective Pictures, Facial Stimuli, Mental States, and Social Language. The Late Positive Potential was the most analyzed in Affective Pictures and was reported to be positively correlated with cognitive and affective empathy, along with other late components. In contrast, for Facial Stimuli, early components presented significant correlations with empathy scales. Particularly, the N170 presented negative correlations with cognitive and affective empathy. Finally, augmented N400 was suggested to be associated with higher empathy scores in the Mental States and Social Language categories. These findings highlight the relevance of early perceptual stages of empathic processing and how different EEG/ERP methodologies provide relevant information.

Effects of aging on face processing: An ERP study of the own-age bias with neutral and emotional faces.

Older adults systematically show an enhanced N170 amplitude during the visualization of facial expressions of emotion. The present study aimed to replicate this finding, further investigating if this effect is specific to facial stimuli, present in other neural correlates of face processing, and modulated by own-age faces. To this purpose, younger (n = 25; Mage = 28.36), middle-aged (n = 23; Mage = 48.74), and older adults (n = 25; Mage = 67.36) performed two face/emotion identification tasks during an EEG recording. The results showed that groups did not differ regarding P100 amplitude, but older adults had increased N170 amplitude for both facial and non-facial stimuli. The event-related potentials analysed were not modulated by an own-age bias, but older faces elicited larger N170 in the Emotion Identification Task for all groups. This increased amplitude may reflect a higher ambiguity of older faces due to age-related changes in their physical features, which may elicit higher neural resources to decode. Regarding P250, older faces elicited decreased amplitudes than younger faces, which may reflect a reduced processing of the emotional content of older faces. This interpretation is consistent with the lower accuracy obtained for this category of stimuli across groups. These results have important social implications and suggest that aging may hamper the neural processing of facial expressions of emotion, especially for own-age peers.

Effects of Concomitant Benzodiazepines and Antidepressants Long-Term Use on Social Decision-Making: Results From the Ultimatum Game.

Benzodiazepines and antidepressants have been shown to change responses to unfairness; however, the effects of their combined use on unfairness evaluation are unknown. This study examines the effects of concomitant benzodiazepines and antidepressants long-term use on the evaluation of fair and unfair offers. To analyze behavioral changes on responses to unfairness, we compared the performance of medicated participants and healthy controls in the Ultimatum Game (UG), both in the proposer and in the respondent role. The results showed that long-term psychotropic users had the worse economic strategy by accepting less offers than control subjects. However, in the proposer role, the unfair offers made by participants were similar between groups. The present results suggest that long-term use of psychotropic medication, specifically the combination of benzodiazepines and antidepressants, may increase the sensitivity to unfairness, resulting in higher rejection rates in conditions where this strategy is the most disadvantageous.

Activation of adenosine A3 receptors regulates vitamin C transport and redox balance in neurons.

Adenosine is an important neuromodulator in the CNS, regulating neuronal survival and synaptic transmission. The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Here we studied the interplay between the adenosinergic system and ascorbate transport in neurons. We found that selective activation of A3, but not of A1 or A2a, adenosine receptors modulated ascorbate transport, decreasing intracellular ascorbate content. Förster resonance energy transfer (FRET) analyses showed that A3 receptors associate with the ascorbate transporter SVCT2, suggesting tight signaling compartmentalization between A3 receptors and SVCT2. The activation of A3 receptors increased ascorbate release in an SVCT2-dependent manner, which largely altered the neuronal redox status without interfering with cell death, glycolytic metabolism, and bioenergetics. Overall, by regulating vitamin C transport, the adenosinergic system (via activation of A3 receptors) can regulate ascorbate bioavailability and control the redox balance in neurons.

Effects of benzodiazepines administration on identification of facial expressions of emotion: a meta-analysis.

RATIONALE: Benzodiazepines, a class of commonly prescribed drugs, were shown to cause cognitive impairments in several domains. However, the effect of benzodiazepines on social cognition is still unclear. OBJECTIVES: In order to clarify how benzodiazepines administration affects the identification of facial expressions of emotion (FEE), we conducted a meta-analysis of 8 empirical studies (N = 153 benzodiazepines, N = 153 placebo). RESULTS: Results showed that participants receiving benzodiazepines were less accurate at identifying facial expressions of anger compared with those receiving placebo (M = - 0.52). Regarding the remaining facial expressions, the meta-analysis did not reveal significant differences between the groups. CONCLUSIONS: We discuss several factors that may explain the differences in the identification of emotions in facial expressions associated with benzodiazepines administration. Additionally, the relevance of assessing the effects of benzodiazepines when used on a long-term basis is addressed.

Understanding the development of face and emotion processing under a predictive processing framework.

In the present work, we explore the development of processing of emotional facial configurations under a predictive processing (or predictive coding) framework. Predictive processing provides a new approach to brain function that has been used to explain a wide range of processes, from perception to socioemotional processing. The explanatory power of this framework for adult brain function is widely recognized, but it has yet to be systematically applied to understanding the developing brain. Studying the findings of developmental research under this framework may allow a deeper understanding of the predictive mechanisms and their ontogenetic course, and adds to knowledge on brain functions and developmental processes. Therefore, the goal of this work was to explore the potential complementarity of predictive processing and development. Specifically, we focus on how the development of facial and emotion processing may be understood under a predictive processing framework. The processing of facial expressions was selected because of the developmental relevance of these stimuli, their impact on general emotional development, as well as the large body of literature on this topic (comprised of both well-established but also incongruent findings, which a novel approach may clarify). Considering the main findings of developmental research on the processing of emotion-related facial configurations under this framework, we argue that predictive processing is consistent with developmental evidence and provides a promising avenue for developmental research, as it reveals new questions in the fields of development and emotion processing. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Antisocial behaviour and psychopathy: Uncovering the externalizing link in the P3 modulation.

In 2009, Gao and Raine's meta-analysis analysed P3 modulation over the antisocial spectrum. However, some questions remained open regarding the P3 modulation patterns across impulsive and violent manifestations of antisocial behaviour, phenotypic components of psychopathy, and P3 components. A systematic review of 36 studies was conducted (N=3514) to extend previous results and to address these unresolved questions. A clear link between decreased P3 amplitude and antisocial behaviour was found. In psychopathy, dimensional approaches become more informative than taxonomic models. Distinct etiological pathways of psychopathy were evidenced in cognitive tasks: impulsive-antisocial psychopathic traits mainly predicted blunted P3 amplitude, while interpersonal-affective psychopathic traits explained enhanced P3 amplitude. Supporting the low fear hypothesis, the interpersonal-affective traits were associated with reduced P3 amplitude in emotional-affective learning tasks. From the accumulated knowledge we propose a framework of P3 amplitude modulation that uncovers the externalizing link between psychopathy and antisocial behaviour. However, the main hypotheses are exploratory and call for more data before stablishing robust conclusions.

Adenosine transporters and receptors: key elements for retinal function and neuroprotection.

Adenosine is an important neuroactive substance in the central nervous system, including in the retina where subclasses of adenosine receptors and transporters are expressed since early stages of development. Here, we review some evidence showing that adenosine plays important functions in the mature as well as in the developing tissue. Adenosine transporters are divided into equilibrative and concentrative, and the major transporter subtype present in the retina is the ENT1. This transporter is responsible for a bidirectional transport of adenosine and the uptake or release of this nucleoside appears to be regulated by different signaling pathways that are also controlled by activation of adenosine receptors. Adenosine receptors are also key players in retina physiology regulating a variety of functions in the mature and developing tissue. Regulation of excitatory neurotransmitter release and neuroprotection are the main functions played be adenosine in the mature tissue, while regulation of cell survival and neurogenesis are some of the functions played by adenosine in developing retina. Since adenosine is neuroprotective against excitotoxic and metabolic dysfunctions observed in neurological and ocular diseases, the search for adenosine-related drugs regulating adenosine transporters and receptors can be important for advancement of therapeutic strategies against these diseases.

Comparison between conventional and real-time PCR assays for diagnosis of visceral leishmaniasis.

The diagnosis of visceral leishmaniasis (VL) is a challenging issue and several studies worldwide have evaluated the different tools to reach a diagnostic solution. The polymerase chain reaction (PCR) has proven to be effective in detecting the genome of Leishmania species in different biological samples. In this study, we compared the conventional PCR and real-time PCR using the Sybr Green system and their application in molecular diagnosis of visceral leishmaniasis in peripheral blood as a biological sample. The genus-specific conserved region of kinetoplast DNA (kDNA) was the target of amplification. We studied 30 samples from patients with suspect of visceral leishmaniasis who were treated by the Medical Clinic of Santa Casa de Belo Horizonte Hospital, Brazil. Among the samples studied, 19 had a confirmed diagnosis for VL by serology and/or by clinical findings. Among these 19 samples, 63% (n = 12) presented positive results for serology and 79% (n = 15) positive results in both PCR methodologies. This fact suggests that the PCR technique can assist in the diagnosis of visceral leishmaniasis in patients who do not have detectable antibodies by serology but can present the genome of the parasite circulating in whole blood. Also, it was possible to observe that there was conformity between the results of the techniques of cPCR and qPCR using the Sybr Green system in 100% of samples analyzed. These data suggest that both PCR techniques were equally effective for detection of the genome of the parasite in the patient's blood.

Modulation of A1 adenosine receptor expression by cell aggregation and long-term activation of A2a receptors in cultures of avian retinal cells: involvement of the cyclic AMP/PKA pathway.

The expression of A1 and A2a adenosine receptors is developmentally regulated in the chick retina, but little is known about the factors important for this regulation. Here, we show that cell aggregation and cAMP analogs promote a dramatic increase in A1 receptor expression. Importantly, a long-term stimulation of A2a receptors also promotes an increase of A1 receptor expression accompanied by a down-regulation of A2a receptors. Chick embryo retina cultures grown in the form of aggregates or dispersed cells accumulate cAMP when stimulated with dopamine or the adenosine agonist 2-chloroadenosine. However, inhibition of dopamine-dependent cAMP accumulation by 2-chloroadenosine was observed in aggregate cultures but not in dispersed cell cultures. Accordingly, A1 receptor binding sites were detected in aggregate cultures, but were low or absent from dispersed cell cultures. Interestingly, an increase of A1 binding sites was detected when dispersed cell cultures were treated for 5 days with permeable cAMP analogs, the adenylyl cyclase activator forskolin or A2a receptor agonists. Although a significant amount of A1 receptor protein was detected in dispersed cell cultures by western blot or immunocytochemistry, the long-term stimulation of A2a receptors also promoted an increase of the A1 receptor protein and mRNA, indicating that A2a receptors and cAMP were regulating transcription and/or translation of A1 receptors. We also found an increase of A1 receptors in locations in or near the membrane after treatment with A2a agonist. The long-term stimulation of retinal explants with A2a agonist also promoted an increase of A1 receptor protein. The results indicate that A2a receptors and the cAMP-dependent protein kinase pathway are involved in the regulation of A1 receptor expression during retinal development.

Activation of glutamate receptors promotes a calcium-dependent and transporter-mediated release of purines in cultured avian retinal cells: possible involvement of calcium/calmodulin-dependent protein kinase II.

Calcium-dependent release of purines was previously demonstrated in cultures of chick retinal cells stimulated with high potassium concentrations but there is no evidence for an exocytotic mechanism of adenosine release from presynaptic terminals. Here we show that activation of NMDA or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate glutamate ionotropic receptors promotes a two- to three-fold increase in the release of purines from these cultures. Approximately 96% of intracellular radioactivity is found as nucleotides after incubation with [(3)H]adenosine, but more than 85% of glutamate-stimulated released material is found as inosine (60%), hypoxanthine (19.9%) and adenosine (7.8%). The release is prevented by removal of extracellular calcium, by the transporter blocker nitrobenzylthioinosine, or inhibitors of calcium/calmodulin-dependent protein kinase II (CAMK II). The uptake of [(3)H]adenosine, but not of [(3)H]GABA or [(3)H]choline, is also blocked by 1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-l-tyrosyl]-4-phenylpiperazine (KN62), N-[2-(N-(4-chlorocinnamyl)-N-methylaminomethyl)phenyl-N-[2-hydroxiethyl]-4-methoxybenzenesulfonamide (KN93) or the myristoylated autocamtide-2-related inhibitory peptide, suggesting that the enzyme modulates the nucleoside transporter. The distribution of intracellular purines was not affected by KN62. These results indicate that activation of glutamate receptors triggers the release of purines from retinal cells by a mechanism involving calcium influx, CAMK II and the nitrobenzylthioinosine-sensitive nucleoside transporter. The regulation of adenosine release by glutamate receptors and CAMK II could have important consequences in the presynaptic control of glutamate release.