Emotional Modulation of Attention: Fear Increases but Disgust Reduces the Attentional Blink

Background

It is well known that facial expressions represent important social cues. In humans expressing facial emotion, fear may be configured to maximize sensory exposure (e.g., increases visual input) whereas disgust can reduce sensory exposure (e.g., decreases visual input). To investigate whether such effects also extend to the attentional system, we used the “attentional blink” (AB) paradigm. Many studies have documented that the second target (T2) of a pair is typically missed when presented within a time window of about 200–500 ms from the first to-be-detected target (T1; i.e., the AB effect). It has recently been proposed that the AB effect depends on the efficiency of a gating system which facilitates the entrance of relevant input into working memory, while inhibiting irrelevant input. Following the inhibitory response on post T1 distractors, prolonged inhibition of the subsequent T2 is observed. In the present study, we hypothesized that processing facial expressions of emotion would influence this attentional gating. Fearful faces would increase but disgust faces would decrease inhibition of the second target.

Methodology/Principal Findings

We showed that processing fearful versus disgust faces has different effects on these attentional processes. We found that processing fear faces impaired the detection of T2 to a greater extent than did the processing disgust faces. This finding implies emotion-specific modulation of attention.

Conclusions/Significance

Based on the recent literature on attention, our finding suggests that processing fear-related stimuli exerts greater inhibitory responses on distractors relative to processing disgust-related stimuli. This finding is of particular interest for researchers examining the influence of emotional processing on attention and memory in both clinical and normal populations. For example, future research could extend upon the current study to examine whether inhibitory processes invoked by fear-related stimuli may be the mechanism underlying the enhanced learning of fear-related stimuli.     

Disgust versus Lust: Exploring the Interactions of Disgust and Fear with Sexual Arousal in Women

Sexual arousal is a motivational state that moves humans toward situations that inherently pose a risk of disease transmission. Disgust is an emotion that adaptively moves humans away from such situations. Incongruent is the fact that sexual activity is elementary to human fitness yet involves strong disgust elicitors. Using an experimental paradigm, we investigated how these two states interact. Women (final N=76) were assigned to one of four conditions: rate disgust stimuli then watch a pornographic clip; watch a pornographic clip then rate disgust stimuli; rate fear stimuli then watch a pornographic clip; or watch a pornographic clip then rate fear stimuli. Women’s genital sexual arousal was measured with vaginal photoplethysmography and their disgust and fear reactions were measured via self-report. We did not find that baseline disgust propensity predicted sexual arousal in women who were exposed to neutral stimuli before erotic content. In the Erotic-before-Disgust condition we did not find that sexual arousal straightforwardly predicted decreased image disgust ratings. However, we did find some evidence that sexual arousal increased self-reported disgust in women with high trait disgust and sexual arousal decreased self-reported disgust in women with low trait disgust. Women who were exposed to disgusting images before erotic content showed significantly less sexual arousal than women in the control condition or women exposed to fear-inducing images before erotic content. In the Disgust-before-Erotic condition the degree of self-reported disgust was negatively correlated with genital sexual arousal. Hence, in the conflict between the ultimate goals of reproduction and disease avoidance, cues of the presence of pathogens significantly reduce the motivation to engage in mating behaviors that, by their nature, entail a risk of pathogen transmission.     

The Divergent Effects of Fear and Disgust on Inhibitory Control: An ERP Study

Negative emotional stimuli have been shown to attract attention and impair executive control. However, two different types of unpleasant stimuli, fearful and disgusting, are often inappropriately treated as a single category in the literature on inhibitory control. Therefore, the present study aimed to investigate the divergent effects of fearful and disgusting distracters on inhibitory control (both conscious and unconscious inhibition). Specifically, participants were engaged in a masked Go/No-Go task superimposed on fearful, disgusting, or neutral emotional contexts, while event-related potentials were measured concurrently. The results showed that for both conscious and unconscious conditions, disgusting stimuli elicited a larger P2 than fearful ones, and the difference waves of P3 amplitude under disgusting contexts were smaller than that under fearful contexts. These results suggest that disgusting distracters consume more attentional resources and therefore impair subsequent inhibitory control to a greater extent. This study is the first to provide electrophysiological evidence that fear and disgust differently affect inhibitory control. These results expand our understanding of the relationship between emotions and inhibitory control.     

The Emotional Brain, Fear, and the Amygdala

1. Considerable progress has been made over the past 20 years in relating specific circuits of the brain to emotional functions. Much of this work has involved studies of Pavlovian or classical fear conditioning, a behavioral procedure that is used to couple meaningless environmental stimuli to emotional (defense) response networks.2. The major conclusion from studies of fear conditioning is that the amygdala plays critical role in linking external stimuli to defense responses.3. Before describing research on the role of the amygdala in fear conditioning, though, it will be helpful to briefly examine the historical events that preceded modern research on conditioned fear.     

Emotional Eating,Alexithymia, and Binge‐Eating Disorder in Obese Women

Objective: To investigate the relationships between alexithymia and emotional eating in obese women with or without Binge Eating Disorder (BED). Research Methods and Procedures: One hundred sixty‐nine obese women completed self‐report questionnaires, including the Beck Depression Inventory, the State Trait Anxiety Inventory, the Stress Perceived Scale, the Dutch Eating Behaviour Questionnaire, and the Toronto Alexithymia Scale. The presence of BED, screened using the Questionnaire of Eating and Weight Patterns, was confirmed by interview. Results: Forty obese women were identified as having BED. BED subjects and non‐BED subjects were comparable in age, body mass index, educational level, and socioeconomic class. According to the Dutch Eating Behaviour Questionnaire, BED subjects exhibited higher depression, anxiety, perceived stress, alexithymia scores, and emotional and external eating scores than non‐BED subjects. Emotional eating and perceived stress emerged as significant predictors of BED. The relationships between alexithymia and emotional eating in obese subjects differed between the two groups according to the presence of BED. Alexithymia was the predictor of emotional eating in BED subjects, whereas perceived stress and depression were the predictors in non‐BED subjects. Discussion: This study pointed out different relationships among mood, alexithymia, and emotional eating in obese subjects with or without BED. Alexithymia was linked to emotional eating in BED. These data suggest the involvement of alexithymia in eating disorders among obese women.     

Dissociation of Learned Helplessness and Fear Conditioning in Mice: A Mouse Model of Depression

The state of being helpless is regarded as a central aspect of depression, and therefore the learned helplessness paradigm in rodents is commonly used as an animal model of depression. The term ‘learned helplessness’ refers to a deficit in escaping from an aversive situation after an animal is exposed to uncontrollable stress specifically, with a control/comparison group having been exposed to an equivalent amount of controllable stress. A key feature of learned helplessness is the transferability of helplessness to different situations, a phenomenon called ‘trans-situationality’. However, most studies in mice use learned helplessness protocols in which training and testing occur in the same environment and with the same type of stressor. Consequently, failures to escape may reflect conditioned fear of a particular environment, not a general change of the helpless state of an animal. For mice, there is no established learned helplessness protocol that includes the trans-situationality feature. Here we describe a simple and reliable learned helplessness protocol for mice, in which training and testing are carried out in different environments and with different types of stressors. We show that with our protocol approximately 50% of mice develop learned helplessness that is not attributable to fear conditioning.     

Relationship between Alexithymia and latent trigger points in the upper Trapezius

Background

Latent trigger points (LTrPs) can be activated by future events, leading to pain. Few studies have reported LTrP risk factors. It has been suggested that alexithymia is associated with myofascial pain and diminished awareness of physical sensation. This study was designed to evaluate the relation between alexithymia and LTrPs found the upper trapezius of healthy individuals.

Methods

The correlation between LTrPs and alexithymia, and between LTrPs and depression was analyzed in 160 healthy participants (80 male, mean age: 40.5 years [20 to 66 years]). Each participant was evaluated for potential LTrPs by careful manual examination and completed the Toronto Alexithymia Scale-20 (TAS-20) and the Beck Depression Inventory (BDI) to assess potential alexithymia and depressive symptoms, respectively.

Results

LTrPs were observed in the upper trapezius of 76 participants (47.5%). TAS-20 scores were significantly higher in subjects with LTrPs than without LTrPs (p?<?0.001); in contrast, there was no significant BDI score difference between these groups (p?=?0.451). The LTrP risk for alexithymia was 2.74 (95% confidence interval [95% CI]: 2.10–3.58). There was no correlation between the TAS-20 and BDI scores (correlation coefficient: ?0.04). Significant risk factors associated with LTrPs included the TAS-20 score (odds ratio [OR]: 1.11, 95% CI: 1.07–1.15) and age (OR: 1.05, 95% CI: 1.01–1.09).

Conclusions

Alexithymia was associated with LTrPs in the upper trapezius of healthy individuals, suggesting that it may serve as a useful predictive factor.

Trial registration

UMIN000027468. Registered 23 May 2017(retrospectively registered).

     

How Does Emotional Context Modulate Response Inhibition in Alexithymia: Electrophysiological Evidence from an ERP Study

Background

Alexithymia, characterized by difficulties in identifying and describing feelings, is highly indicative of a broad range of psychiatric disorders. Several studies have also discovered the response inhibition ability impairment in alexithymia. However, few studies on alexithymic individuals have specifically examined how emotional context modulates response inhibition procedure. In order to investigate emotion cognition interaction in alexithymia, we analyzed the spatiao-temporal features of such emotional response inhibition by the approaches of event-related potentials and neural source-localization.

Method

The study participants included 15 subjects with high alexithymia scores on the 20-item Toronto Alexithymia Scale (alexithymic group) and 15 matched subjects with low alexithymia scores (control group). Subjects were instructed to perform a modified emotional Go/Nogo task while their continuous electroencephalography activities were synchronously recorded. The task includes 3 categories of emotional contexts (positive, negative and neutral) and 2 letters (“M” and “W”) centered in the screen. Participants were told to complete go and nogo actions based on the letters. We tested the influence of alexithymia in this emotional Go/Nogo task both in behavioral level and related neural activities of N2 and P3 ERP components.

Results

We found that negatively valenced context elicited larger central P3 amplitudes of the Nogo–Go difference wave in the alexithymic group than in the control group. Furthermore, source-localization analyses implicated the anterior cingulate cortex (ACC) as the neural generator of the Nogo-P3.

Conclusion

These findings suggest that difficulties in identifying feelings, particularly in negative emotions, is a major feature of alexithymia, and the ACC plays a critical role in emotion-modulated response inhibition related to alexithymia.     

Dissociation between aggregation and superoxide production in human granulocytes

Aggregation and the activation of the granulocyte (PMN) superoxide (O2-) generating system occur when certain stimuli are added to resting cells. It had previously been postulated that PMN aggregation is essential for maximal O2- production. This study was undertaken to test the hypothesis that PMN aggregation is required for full expression of PMN O2- production. We examined aggregation and O2- production induced by four stimuli; concanavalin A (Con A), phorbol myristate acetate (PMA), N-formylmethionyl-leucyl-phenylalanine (FMLP), and ionophore A23187. Cytochalasin B enhanced aggregation by all four stimuli but only enhanced the rate of O2- production by Con A; 2-deoxyglucose inhibited aggregation by all stimuli. Dissociation of PMN aggregation and O2- production was achieved by using NEM, TPCK, and divalent cations. NEM and TPCK prevent Con A-induced O2- production but have no effect on Con A-induced aggregation. PMA-stimulated PMN generate O2- in the presence or absence of Ca++ and Mg++. In contrast, PMA stimulated maximum PMN aggregation only in the presence of both Ca++ and Mg++. Thus PMN can generate O2- without aggregating, and PMN can aggregate without producing O2-. PMN from patients with chronic granulomatous disease do not generate O2- or undergo membrane potential depolarization in response to PMA. These PMN aggregated when stimulated with PMA, providing evidence that depolarization is not required for PMN aggregation. We conclude that aggregation and the activation of the O2- generating system, though temporally related, are not necessarily causally related.     

Dissociation between metabolic and vascular insulin resistance in aging

Physiological actions of insulin via activation of the phosphatidylinositol 3-kinase/Akt pathway in the endothelium serve to couple regulation of hemodynamic and metabolic homeostasis. Insulin resistance, endothelial dysfunction, and hypertension increase in prevalence with aging. We investigated the metabolic and endothelial actions of insulin in 24- vs. 3-mo Sprague-Dawley rats. With the use of the hyperinsulinemic euglycemic clamp, the rate of glucose infusion necessary to maintain equivalent plasma glucose (5.5 mmol/l) was similar in 24- vs. 3-mo rats, as was fasting glucose (5.2 +/- 0.33 vs. 4.4 +/- 0.37 mmol/l; mean +/- SE) and insulin (0.862 +/- 0.193 vs. 1.307 +/- 0.230 mg/l). Systolic blood pressure was higher in 24-mo rats (133 +/- 5 vs. 110 +/- 4 mmHg; P = 0.005). Endothelial nitric oxide (NO)-dependent relaxation to insulin was impaired in aortas of 24- vs. 3-mo rats (maximal response 8.9 +/- 4.3 vs. 34.9 +/- 3.9%; P = 0.002); N(G)-nitro-l-arginine methyl ester abolished insulin-mediated relaxation in 3- but not 24-mo rats. Endothelium NO-dependent (acetylcholine) and -independent (sodium nitroprusside) relaxation, as well as NADPH oxidase activity, were similar in 3- and 24-mo rats. Insulin increased aortic serine phosphorylation of Akt in 3-mo rats by 120% over 24-mo rats (P < 0.05) and serine phosphorylation of endothelial NO synthase (eNOS) in 3-mo rats by 380% over 24-mo rats (P < 0.05). Aortic expression of phosphorylated c-Jun NH(2)-terminal kinase-1 and serine phosphorylated insulin receptor substrate-1, known mediators of metabolic insulin resistance, was similar in 3- and 24-mo rats. Expression of caveolin-1, a regulator of eNOS activity and insulin signaling, was 55% lower in 24- than 3-mo rats (P = 0.002). In summary, impaired vasorelaxation to insulin in aging was independent of metabolic insulin sensitivity and associated with impaired insulin-mediated activation of the Akt/eNOS pathway, but intact activation of the acetylcholine-mediated Ca(2+)-calmodulin/eNOS pathway. Vascular insulin resistance in aging may add to the increased susceptibility of this population to vascular injury induced by traditional cardiovascular risk factors.     

Alexithymia and the Processing of Emotional Facial Expressions (EFEs): Systematic Review, Unanswered Questions and Further Perspectives

Alexithymia is characterized by difficulties in identifying, differentiating and describing feelings. A high prevalence of alexithymia has often been observed in clinical disorders characterized by low social functioning. This review aims to assess the association between alexithymia and the ability to decode emotional facial expressions (EFEs) within clinical and healthy populations. More precisely, this review has four main objectives: (1) to assess if alexithymia is a better predictor of the ability to decode EFEs than the diagnosis of clinical disorder; (2) to assess the influence of comorbid factors (depression and anxiety disorder) on the ability to decode EFE; (3) to investigate if deficits in decoding EFEs are specific to some levels of processing or task types; (4) to investigate if the deficits are specific to particular EFEs. Twenty four studies (behavioural and neuroimaging) were identified through a computerized literature search of Psycinfo, PubMed, and Web of Science databases from 1990 to 2010. Data on methodology, clinical characteristics, and possible confounds were analyzed. The review revealed that: (1) alexithymia is associated with deficits in labelling EFEs among clinical disorders, (2) the level of depression and anxiety partially account for the decoding deficits, (3) alexithymia is associated with reduced perceptual abilities, and is likely to be associated with impaired semantic representations of emotional concepts, and (4) alexithymia is associated with neither specific EFEs nor a specific valence. These studies are discussed with respect to processes involved in the recognition of EFEs. Future directions for research on emotion perception are also discussed.     

Dissociation between diaphragmatic and rib cage muscle fatigue

To assess rib cage muscle fatigue and its relationship to diaphragmatic fatigue, we recorded the electromyogram (EMG) of the parasternal intercostals (PS), sternocleidomastoid (SM), and platysma with fine wire electrodes and the EMG of the diaphragm (DI) with an esophageal electrode. Six normal subjects were studied during inspiratory resistive breathing. Two different breathing patterns were imposed: mainly diaphragmatic or mainly rib cage breathing. The development of fatigue was assessed by analysis of the high-to-low (H/L) ratio of the EMG. To determine the appropriate frequency bands for the PS and SM, we established their EMG power spectrum by Fourier analysis. The mean and SD for the centroid frequency was 312 +/- 16 Hz for PS and 244 +/- 48 Hz for SM. When breathing with the diaphragmatic patterns, all subjects showed a fall in H/L of the DI and none had a fall in H/L of the PS or SM. During rib cage emphasis, four out of five subjects showed a fall in H/L of the PS and five out of six showed a fall in H/L of the SM. Four subjects showed no fall in H/L of the DI; the other two subjects were unable to inhibit diaphragm activity to a substantial degree and did show a fall in H/L of the DI. Activity of the platysma was minimal or absent during diaphragmatic emphasis but was usually strong during rib cage breathing. We conclude that fatigue of either the diaphragm or the parasternal and sternocleidomastoid can occur independently according to the recruitment pattern of inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dissociation between IFN-alpha-induced anti-viral and growth signaling pathways

The ability of IFN-alpha to induce an anti-viral state in a wide variety of cell types as well as to inhibit cellular growth has long been appreciated. It is less clear, however, whether both these effects lie downstream of a common signaling pathway. In this study we have taken advantage of an atypical human myeloma cell line (KAS-6/1) displaying a dramatic proliferative response to IFN-alpha in an effort to resolve the signaling requirements for IFN-alpha-induced anti-viral and growth regulatory effects. Thus, we have analyzed the ability of IFN-alpha to induce a number of known receptor-initiated events in this cell line and have compared these responses with those exhibited by a cell lineage- and maturation stage-matched myeloma cell line (ANBL-6) that displays typical IFN-alpha responsiveness. Despite the widely contrasting effects of IFN-alpha on cellular proliferation, IFN-alpha was shown to be comparable in its ability to induce the expression of early response genes as well as induce resistance to viral infection in both cell lines. By contrast, the effects of IFN-alpha on the activation of mitogen-activated protein kinase (MAPK) were strikingly distinct. Finally, although inhibition of MEK and MAPK activation had no effect on the induction of the anti-viral response, it completely blocked IFN-alpha-stimulated proliferation of the KAS-6/1 cells. In summary, our analysis of the role of the MAPK and anti-viral signaling pathways using these two cell lines suggests that the anti-viral and growth regulatory effects of IFN-alpha display a differential requirement for activation of the MAPK pathway.     

Dissociation between inositol polyphosphate production and mitogenesis in mouse thymocytes

Cortical and medullary thymocytes can be separated from each other by virtue of the fact that only cortical thymocytes bear peanut agglutinin (PNA) receptors. The mitogenic responses of subpopulations of thymocytes were studied. We have confirmed the results of Conlon et al. [(1982) J. Immun. 128, 797-801], that lectin-induced stimulation of unseparated cells, and PNA- but not PNA+ thymocytes, results in DNA synthesis. In contrast, both subpopulations, as well as unseparated cells, synthesize DNA in response to the calcium ionophore A23187 in the presence of the phorbol ester TPA, suggesting an impairment of signal transduction in PNA+ cells. However, comparable amounts of inositol phosphates were accumulated in PNA- and PNA+ thymocytes in response to Concanavalin A (Con A). We suggest that mitogenic lectins generate a third signal in addition to elevation of intracellular free calcium concentration and activation of protein kinase C. This signal is generated in PNA- but not in PNA+ thymocytes and is obligatory for lectin-induced stimulation.     

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia

The objective of this study was to quantitatively assess changes in cell adhesion molecule (CAM) expression on the pulmonary endothelial surface during hyperoxia and to assess the functional significance of those changes on cellular trafficking and development of oxygen-induced lung injury. Mice were placed in >95% O(2) for 0-72 h, and pulmonary injury and neutrophil (PMN) sequestration were assessed. Specific pulmonary CAM expression was quantified with a dual-radiolabeled MAb technique. To test the role of CAMs in PMN trafficking during hyperoxia, blocking MAbs to murine P-selectin, ICAM-1, or platelet-endothelial cell adhesion molecule-1 (PECAM-1) were injected in wild-type mice. Mice genetically deficient in these CAMs and PMN-depleted mice were also evaluated. PMN sequestration occurred within 8 h of hyperoxia, although alveolar emigration occurred later (between 48 and 72 h), coincident with rapid escalation of the lung injury. Hyperoxia significantly increased pulmonary uptake of radiolabeled antibodies to P-selectin, ICAM-1, and PECAM-1, reflecting an increase in their level on pulmonary endothelium and possibly sequestered blood cells. Although both anti-PECAM-1 and anti-ICAM-1 antibodies suppressed PMN alveolar influx in wild-type mice, only mice genetically deficient in PECAM-1 showed PMN influx suppression. Neither CAM blockade, nor genetic deficiency, nor PMN depletion attenuated lung injury. We conclude that early pulmonary PMN retention during hyperoxia is not temporally associated with an increase in endothelial CAMs; however, subsequent PMN emigration into the alveolar space may be supported by PECAM-1 and ICAM-1. Blocking PMN recruitment did not prevent lung injury, supporting dissociation between PMN infiltration and lung injury during hyperoxia in mice.     

Dissociation between hysteresivity and tension in constricted tracheal and parenchymal strips

The object of this study was to investigatehow changes in the contractile state of smooth muscle would modifyoscillatory mechanics of tracheal muscle and lung parenchyma duringagonist challenge. Guinea pig tracheal and parenchymal lung strips were suspended in an organ bath. Measurements of length(L) and tension (T) were recordedduring sinusoidal oscillations under baseline conditions and afterchallenge with 1 mM ACh. Measurements were also obtained in stripspretreated with the calmodulin inhibitor calmidazolium (Cmz) orstaurosporine (Stauro), a protein kinase C inhibitor. Elastance (E) andresistance (R) were calculated by fitting changes in T,L, andL/tto the equation of motion. Hysteresivity () was obtained from thefollowing equation: = (R/E)2f,where f is frequency. Finally, maximalunloaded shortening velocity during electrical field stimulation wasmeasured in Cmz-pretreated and control tracheal strips. In trachealstrips, pretreatment with Cmz caused a significant decrease in the  response to ACh challenge and in maximal unloaded shortening velocitymeasured during electrical field stimulation; Stauro decreased the T,E, and R response to ACh. In parenchymal strips, Cmz decreased the  response, whereas Stauro had no effect. These results suggest thatmodifications in the contractile state of the smooth muscle arereflected in changes in the hysteretic behavior and that T and  maybe controlled independently. Second, inasmuch as changes in  weresimilar in parenchymal and tracheal strips, the contractile element isimplicated as the structure responsible for constriction-induced changes in the mechanical behavior of the lung periphery.

     

Dissociation between cholesterol secretion and plasma lipid transfer activity in rabbits

Human and rabbit plasma contains a lipid transfer protein that transfers cholesteryl esters and triglycerides among the plasma lipoproteins and may also have a role in the movement of lipids into and out of cells. Little is known about the regulation of the activity of the lipid transfer protein, but in the rabbit, hypercholesterolemia is associated with increased plasma lipid transfer activity (LTA). Perfused rabbit livers secrete LTA, and hepatic cholesterol secretion is increased in rabbits with diet-induced hypercholesterolemia. Thus, experiments were performed with rabbits to determine if LTA is regulated by a concerted hepatic secretion of lipoprotein protein cholesterol and LTA. Rabbits were fed chow or chow plus coconut oil (14% wt/wt), and plasma lipids, LTA, and the rate of secretion of cholesterol into plasma were determined. Coconut oil feeding increased plasma cholesterol by 68%, LTA by 42%, and hepatic cholesterol secretion by 69%. Mevinolin (75 mg/day), an inhibitor of cholesterol biosynthesis, lowered LTA and plasma cholesterol without affecting the rate of secretion of cholesterol into plasma. These studies provide further evidence that, in the rabbit, plasma cholesterol and LTA are closely related, and the association is not likely to be caused by a concerted hepatic secretion of cholesterol and LTA.