Regulation Of Affective States Research Articles

Cognitive flexibility and emotion regulation: Dual layers of resilience against the emergence of paranoia

Cognitive inflexibility has been linked to difficulties in revising paranoid beliefs, whereas cognitive flexibility may protect against the development and maintenance of paranoid beliefs by allowing for troubleshooting in light of available evidence. While less discussed in the context of paranoia research, better regulation of affective states may reduce the likelihood of biased beliefs developing in the first place, reducing the burden on belief updating mechanisms. The present study hypothesized that high cognitive flexibility and strong emotion regulation ability may act as a reciprocal protective shield against the risk associated with lower ability in the other domain. Participants were recruited from the general population (N = 221) to complete the Ambiguous Interpretation Inflexibility Task, as well as self-report measures for paranoia and emotion regulation ability. The results show an interaction between cognitive flexibility and emotion regulation ability as related to less severe paranoia. Better emotion regulation ability is associated with lower paranoia in individuals with lower cognitive flexibility, whereas higher cognitive flexibility is associated with less severe paranoia in individuals with greater emotion regulation difficulties. These findings highlight the importance of emotion regulation in early interventions of paranoia, especially how emotion regulation relates to known cognitive vulnerabilities such as inflexibility.

Reduced emission of alarm 22-kHz ultrasonic vocalizations during fear conditioning in rats lacking the serotonin transporter

Rats display a rich social behavioral repertoire. An important component of this repertoire is the emission of whistle-like calls in the ultrasonic range, so-called ultrasonic vocalizations (USV). Long low-frequency 22-kHz USV occur in aversive situations, including aggressive interactions, predator exposure, and electric shocks during fear conditioning. They are believed to reflect a negative affective state akin to anxiety and fear. A prominent theory suggests that 22-kHz USV function as alarm calls to warn conspecifics. Serotonin (5-hydroxytryptamine, 5-HT) is strongly implicated in the regulation of affective states, particularly anxiety and fear. A key component of the system is the 5-HT transporter (5-HTT, also known as SERT), regulating 5-HT availability in the synaptic cleft. In the present experiment, we studied the effects of SERT deficiency on overt fear-related behavior and alarm 22-kHz USV during fear conditioning in male and female rats. While overt fear-related behavior was not affected by SERT deficiency and sex, the emission of alarm 22-kHz USV was clearly reduced in homozygous SERT−/− but not heterozygous SERT+/− mutants, as compared to their wildtype SERT+/+ littermate controls. Genotype effects were particularly prominent in females. Females in general emitted fewer alarm 22-kHz USV than males. This supports the view that 22-kHz USV are, at least partly, independently regulated from anxiety or fear and as socially mediated alarm calls do not simply express a negative affective state. Reduced 22-kHz USV emission in rats lacking SERT might be due to social deficits in the use of 22-kHz USV as a socio-affective signal to warn conspecifics about threats.

Whatever happened to multiple complex developmental disorder?

Multiple complex developmental disorder is characterized by early-onset combined impairment in the regulation of affective states, in the social behavior, and in the thought processes. First described in the Eighties, so far multiple complex developmental disorder has so far not found recognition as an autonomous nosographic entity in international classifiers. In the past, the most common diagnosis for patients presenting with this clinical picture was that of ‘pervasive developmental disorder not otherwise specified,’ due to the early-onset impairment in various development areas, including the social functioning, with pervasive characteristics. Over recent years, based on literature data, the interest in multiple complex developmental disorder has seemed to decline. Yet, several clinical and neurobiological findings emerging from the literature seem to support the nosographic autonomy of multiple complex developmental disorder. The correct recognition of this clinical picture appears to be of considerable importance because children who are affected seem to be predisposed to develop a schizophrenia spectrum disorder during their lifetime. Multiple complex developmental disorder could be a very interesting entity, being a possible kind of “bridge” condition between autism spectrum disorder and childhood-onset schizophrenia. However, there is a lack of findings of the real recurrence, neurobiologic background, and course of this clinical picture.

Gradient of Expression of Dopamine D2 Receptors Along the Dorso-Ventral Axis of the Hippocampus.

Dopamine D2-like receptors (D2R) play an important role in the regulation of hippocampal neuronal excitability and contribute to the regulation of synaptic plasticity, the encoding of hippocampus-dependent memories and the regulation of affective state. In line with this, D2R are targeted in the treatment of psychosis and affective disorders. It has been proposed that the dorso-ventral axis of the hippocampus can be functionally delineated into the dorsal pole that predominantly processes spatial information and the ventral pole that mainly addresses hippocampal processing of emotional and affective state. Although dopaminergic control of hippocampal information processing has been the focus of a multitude of studies, very little is known about the precise distribution of D2R both within anatomically defined sublayers of the hippocampus and along its dorsoventral axis, that could in turn yield insights as to the functional significance of this receptor in supporting hippocampal processing of spatial and affective information. Here, we used an immunohistochemical approach to precisely scrutinize the protein expression of D2R both within the cellular and dendritic layers of the hippocampal subfields, and along the dorso-ventral hippocampal axis. In general, we detected significantly higher levels of protein expression of D2R in the ventral, compared to the dorsal poles with regard to the CA1, CA2, CA3 and dentate gyrus (DG) regions. Effects were very consistent: the molecular layer, granule cell layer and polymorphic layer of the DG exhibited higher D2R levels in the ventral compared to dorsal hippocampus. D2R levels were also significantly higher in the ventral Stratum oriens, Stratum radiatum, and Stratum lacunosum-moleculare layers of the CA1 and CA3 regions. The apical dendrites of the ventral CA2 region also exhibited higher D2R expression compared to the dorsal pole. Taken together, our study suggests that the higher D2R expression levels of the ventral hippocampus may contribute to reported gradients in the degree of expression of synaptic plasticity along the dorso-ventral hippocampal axis, and may support behavioral information processing by the ventral hippocampus.

Introducing Temporal Theory to the Field of Sport Psychology: Toward a Conceptual Model of Time Perspectives in Athletes' Functioning.

Time perspective theory provides a robust conceptual framework for analyzing human behavior in the context of time. So far, the concept has been studied and applied in multiple life domains, such as education, health, social relationships, environmental behavior, or financial behavior; however, its explanatory potential has been completely neglected within the domain of sport. In the present paper we provide a deepened theoretical analysis of the potential role of temporal framing of human experience for sport-related attitudes, emotions, and athletic performance. We propose a conceptual model in which time perspectives influence psychological functioning and performance of athletes via three major mechanisms: (1) magnitude and persistence of sport motivation and resulting athlete engagement, (2) regulation of affective states during sport performance, and (3) appraisal of one’s performance and coping with resulting emotions. We support the theoretical considerations based on the major assumptions of time perspective theory with research findings regarding the regulatory role of time perspectives in other life domains. We also highlight potential research paths that would allow us to empirically test the present model and determine the actual role of temporal perspectives in shaping crucial aspects of athletes’ psychological functioning, as well as levels of their sport performance.

Borderline personality disorder and bias in the recognition of facial expressions of emotion: a pathway to understand the psychopathology

Background The identification of facial emotions is a key skill as it promotes rapid and accurate recognition of emotions and enables better communication and greater social adaptation. More recent studies have suggested that impaired social interactions may be related to deficits in social cognition and therefore in the recognition of facial expressions, contributing to social disturbance among individuals with borderline personality disorder (BPD). Objective To present the results of an empirical study assessing the recognition of facial emotion expressions in women with BPD, having as reference a group of healthy women from the general population. Methods The subjects (40 female with BPD and 40 controls) were assessed with a dynamic task on a computer screen for recognition of facial expressions of emotion. Results The BPD group had a lower accuracy in perceiving emotions of fear and surprise and slowness in recognising happiness. Logistic regression analyses also identified an association between BPD and higher sensitivity in the recognition of anger. Discussion Women with BPD made more mistakes in the recognition of negative emotions, which can bias the behaviour and regulation of affective states, favouring in turn the emergence of some typical symptoms associated with BPD.

Effects of cognitive control training on the dynamics of (mal)adaptive emotion regulation in daily life.

Cognitive control plays a key role in both adaptive emotion regulation, such as positive reappraisal, and maladaptive emotion regulation, such as rumination, with both strategies playing a major role in resilience and well-being. As a result, cognitive control training (CCT) targeting working memory functioning may have the potential to reduce maladaptive emotion regulation and increase adaptive emotion regulation. The current study explored the effects of CCT on positive reappraisal ability in a lab context, and deployment and efficacy of positive appraisal and rumination in daily life. A sample of undergraduates (n = 83) was allocated to CCT or an active control condition, performing 10 online training sessions over a period of 14 days. Effects on regulation of affective states in daily life were assessed using experience sampling over a 7-day posttraining period. Results revealed a positive association between baseline cognitive control and self-reported use of adaptive emotion regulation strategies, whereas maladaptive emotion regulation strategies showed a negative association. CCT showed transfer to working memory functioning on the dual n-back task. Overall, effects of CCT on emotion regulation were limited to reducing deployment of rumination in low positive affective states. However, we did not find beneficial effects on indicators of adaptive emotion regulation. These findings are in line with previous studies targeting maladaptive emotion regulation but suggest limited use in enhancing adaptive emotion regulation in a healthy sample. (PsycINFO Database Record

Dissociating Bottom-Up and Top-Down Mechanisms in the Cortico-Limbic System during Emotion Processing.

The cortico-limbic system is critically involved in emotional responses and resulting adaptive behaviors. Within this circuit, complementary regions are believed to be involved in either the appraisal or the regulation of affective state. However, the respective contribution of these bottom-up and top-down mechanisms during emotion processing remains to be clarified. We used a new functional magnetic resonance imaging (fMRI) paradigm varying 3 parameters: emotional valence, emotional congruency, and allocation of attention, to distinguish the functional variation in activity and connectivity between amygdala, anterior cingulate cortex (ACC), and dorsolateral prefrontal cortex (DLPFC). Bottom-up appraisal of negative compared with positive stimuli led to a greater amygdala response and stronger functional interaction between amygdala and both dorsal ACC and DLPFC. Top-down resolution of emotional conflict was associated with increased activity within ACC and higher functional connectivity between this structure, and both the amygdala and DLPFC. Finally, increased top-down attentional control caused greater engagement of the DLPFC, accompanied by increased connectivity between DLPFC and dorsal ACC. This novel task provides an efficient tool for exploring bottom-up and top-down processes underlying emotion and may be particularly helpful for investigating the neurofunctional underpinnings of psychiatric disorders.

Are happy children socially successful? Testing a central premise of positive psychology in a sample of preschool children

Current developmental studies of affect/emotion emphasize knowledge about and regulation of affective states and/or behaviors. Expressiveness per se is rarely studied independently from knowledge and/or regulation; consequently, recent studies of young children's affect do not interface with the literature from positive psychology indicating that the chronic experience of positive affect predicts a range of desirable life outcomes. We assessed affect expressiveness for 377 preschool children in dyadic peer play. Correlation indicated that dyadic positive affect was associated with peer acceptance, visual attention received from peers, rate of initiating positive interactions, and classroom adjustment from teachers’ ratings and that negative affect was associated (negatively) with peer acceptance. Negative affect was also positively associated with teacher-rated dysregulation. Subsequent multi-level regressions showed that positive and negative affect uniquely predicted most of their respective correlates when entered together as Level-1 predictors with dysregulation.

Adult hippocampal neurogenesis is involved in anxiety-related behaviors

Adult hippocampal neurogenesis is a unique example of structural plasticity, the functional role of which has been a matter of intense debate. New transgenic models have recently shown that neurogenesis participates in hippocampus-mediated learning. Here, we show that transgenic animals, in which adult hippocampal neurogenesis has been specifically impaired, exhibit a striking increase in anxiety-related behaviors. Our results indicate that neurogenesis plays an important role in the regulation of affective states and could be the target of new treatments for anxiety disorders.

Dysregulation of Endogenous Opioid Emotion Regulation Circuitry in Major Depression in Women

There is extensive evidence implicating dysfunctions in stress responses and adaptation to stress in the pathophysiological mechanism of major depressive disorder (MDD) in humans. Endogenous opioid neurotransmission activating mu-opioid receptors is involved in stress and emotion regulatory processes and has been further implicated in MDD. To examine the involvement of mu-opioid neurotransmission in the regulation of affective states in volunteers with MDD and its relationship with clinical response to antidepressant treatment. Measures of mu-opioid receptor availability in vivo (binding potential [BP]) were obtained with positron emission tomography and the mu-opioid receptor selective radiotracer carbon 11-labeled carfentanil during a neutral state. Changes in BP during a sustained sadness challenge were obtained by comparing it with the neutral state, reflecting changes in endogenous opioid neurotransmission during the experience of that emotion. Clinics and neuroimaging facilities at a university medical center. Fourteen healthy female volunteers and 14 individually matched patient volunteers diagnosed with MDD were recruited via advertisement and through outpatient clinics. Sustained neutral and sadness states, randomized and counterbalanced in order, elicited by the cued recall of an autobiographical event associated with that emotion. Following imaging procedures, patients underwent a 10-week course of treatment with 20 to 40 mg of fluoxetine hydrochloride. Changes in mu-opioid receptor BP during neutral and sustained sadness states, negative and positive affect ratings, plasma cortisol and corticotropin levels, and clinical response to antidepressant administration. The sustained sadness condition was associated with a statistically significant decrease in mu-opioid receptor BP in the left inferior temporal cortex of patients with MDD and correlated with negative affect ratings experienced during the condition. Conversely, a significant increase in mu-opioid receptor BP was observed in healthy control subjects in the rostral region of the anterior cingulate. In this region, a significant decrease in mu-opioid receptor BP during sadness was observed in patients with MDD who did not respond to antidepressant treatment. Comparisons between patients with MDD and controls showed significantly lower neutral-state mu-opioid receptor BP in patients with MDD in the posterior thalamus, correlating with corticotropin and cortisol plasma levels. Larger reductions in mu-opioid system BP during sadness were obtained in patients with MDD in the anterior insular cortex, anterior and posterior thalamus, ventral basal ganglia, amygdala, and periamygdalar cortex. The same challenge elicited larger increases in the BP measure in the control group in the anterior cingulate, ventral basal ganglia, hypothalamus, amygdala, and periamygdalar cortex. The results demonstrate differences between women with MDD and control women in mu-opioid receptor availability during a neutral state, as well as opposite responses of this neurotransmitter system during the experimental induction of a sustained sadness state. These data demonstrate that endogenous opioid neurotransmission on mu-opioid receptors, a system implicated in stress responses and emotional regulation, is altered in patients diagnosed with MDD.

Disruption of cortical-limbic interaction as a substrate for comorbidity

The prefrontal cortex exerts a potent regulatory influence over subcortical systems that are involved in the regulation of affective states. In particular, the amygdala is a region that is known to play a prominent role in the expression of emotions, and this function is believed to be disrupted in affective disorders and drug abuse. In addition, dysfunction of the prefrontal cortex is believed to be a common element in many psychiatric disorders such as schizophrenia. Using electrophysiological recordings in rodents, we examined the interactions of the prefrontal cortex with the amygdala. Our studies showed that these areas are strongly interdependent, with the prefrontal cortex showing conditioned responses that depend on amygdala inputs, and in turn exerting a potent attenuation of activity within the amygdala. In particular, the ability of the prefrontal cortex to modulate amygdala activity is likely to play an important role in our ability to cope with stressors. We propose that a dysfunction within the prefrontal cortex disrupts the ability of this region to effectively modulate the amygdala, leaving the organism susceptible to detrimental effects of stressors. This would appear to be a common underlying process that may leave the individual susceptible to drug abuse and to the onset or exacerbation of psychiatric disorders such as schizophrenia and depression.

Regulation of Human Affective Responses by Anterior Cingulate and Limbic µ-Opioid Neurotransmission

Human affective responses appear to be regulated by limbic and paralimbic circuits. However, much less is known about the neurochemical systems engaged in this regulation. The mu-opioid neurotransmitter system is distributed in, and thought to regulate the function of, brain regions centrally implicated in affective processing. To examine the involvement of mu-opioid neurotransmission in the regulation of affective states in healthy human volunteers. Measures of mu-opioid receptor availability in vivo were obtained with positron emission tomography and the mu-opioid receptor selective radiotracer [11C]carfentanil during a neutral state and during a sustained sadness state. Subtraction analyses of the binding potential maps were then performed within subjects, between conditions, on a voxel-by-voxel basis. Imaging center at a university medical center. Fourteen healthy female volunteers. Intervention Sustained neutral and sadness states, randomized and counterbalanced in order, elicited by the cued recall of an autobiographical event associated with that emotion. Changes in mu-opioid receptor availability and negative and positive affect ratings between conditions. Increases or reductions in the in vivo receptor measure reflect deactivation or activation of neurotransmitter release, respectively. The sustained sadness condition was associated with a statistically significant deactivation in mu-opioid neurotransmission in the rostral anterior cingulate, ventral pallidum, amygdala, and inferior temporal cortex. This deactivation was reflected by increases in mu-opioid receptor availability in vivo. The deactivation of mu-opioid neurotransmission in the rostral anterior cingulate, ventral pallidum, and amygdala was correlated with the increases in negative affect ratings and the reductions in positive affect ratings during the sustained sadness state. These data demonstrate dynamic changes in mu-opioid neurotransmission in response to an experimentally induced negative affective state. The direction and localization of these responses confirms the role of the mu-opioid receptor system in the physiological regulation of affective experiences in humans.

THE ORIGIN AND ORGANIZATION OF SOCIOAFFECTIVE DIALOGUE

This work provides an account of the neuropsychosocial genesis and organization of socioaffective dialogue. Socioaffective dialogue is a mutually reciprocated process of interaction, between two or more individuals, in which the arousal and regulation of affective states generates a co-evolving order of meaning that in-forms (gives shape to) action and behavior. The work is organized in three parts. Part I begins with a description, drawn primarily from Schore's (1994) work, of the neuropsychosocial origins of all social communication which develops in the socioaffective interaction between a mother and her new born infant. The interaction is organized along two dimensions: one involving the stimulation of positive emotional affects, and the second involving the regulation of the infant's aroused affective states. These interactions affect and direct the growth and transformation of the infant's brain and, when optimally organized, produce a stable, self-regulating “dialogical self,” marked by the onset of speech, at around eighteen months. Part II shows that the same two dimensions—affective arousal and control—continue to be operative in the adult world in communication in intimate relationships and in social collectives. A review of Sternberg's (1986) research on love and Bradley's (1987) research on communes reveals that stable social organization is generated when interaction along the two dimensions is coupled as a self-regulating communication system. Part III uses Bradley and Pribrams' (1998) theory of communication to explain this result. The theory views the interaction between the two orders as an information processing system. When optimally organized as socioaffective dialogue, the interaction gathers and communicates holographic-like descriptions of endogenous organization throughout a social unit to in-form collective organization. However, there are limits on the combinations of affective arousal and control which are functional. Failure to maintain combinations within the requisite limits may prevent the creation and distribution of meaning and, hence, jeopardize collective organization.

Review : Gonadal Steroids and Affective Illness

Gonadal steroids seem to regulate affective state in some people (but not all), despite the absence of abnormal steroid hormone levels or dysfunction of the reproductive endocrine axis. In this article, we attempt to explain this paradox 1) by describing the molecular mechanisms by which gonadal steroids can regulate neuronal function; 2) by describing the specific regulatory impact of gonadal steroids on two systems im plicated in the pathophysiology of mood disorders; and 3) by defining the role of gonadal steroids in several mood disorders linked to periods of reproductive change. We suggest that the context in which the neuro- regulatory actions of gonadal steroids occur determines the impact of steroid signaling on the regulation of affective state. NEUROSCIENTIST 5:227-237, 1999

Neuropeptide Y Y 1 receptor antagonist BIBP3226 produces conditioned place aversion in rats

1. 1. Previous studies have shown that the blockade of the neuropeptide Y (NPY) y 1 receptors with N 2- (diphenylacetyl)- N-[(4-hydroxy-phenyl)methyl]-D-arginine amide (BIBP3226) induces anxiogenic-like reaction in rats tested in elevated plus-maze test. 2. 2. The present study examined whether such a treatment is aversive using place conditioning in a two- compartment apparatus. Locomotor activity was measured in open field test. 3. 3. Pairings with potentially anxiogenic dose of BIBP3226 (5μg/6.5μl I.c.v.) produced a conditioned aversion for the drug-associated place, whereas the locomotor activity in the open field test was not affected by this dose of BIBP3226. 4. 4. These data suggest that the blockade of central NPY y 1 receptors is aversive and provide additional evidence to the hypothesis that the NPY y 1 receptors are involved in the regulation of affective states.

Impact of experimentally induced serotonin deficiency by tryptophan depletion on sleep EEC in healthy subjects

The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism. Because serotonin is involved in sleep regulation and the regulation of affective states, we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients. A total of 12 healthy subjects (mean age 34 +/- 3 years) had eight polysomnograms, divided in two blocks of 4 consecutive nights. After one adaptation and 1 baseline night, subjects received a low-protein diet on day 3 and 4 until midday. On day 4 at 18.00 h, they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan (placebo control) in randomized and double-blind order, resulting in an 85% decrease (tryptophan depletion) and a 144% increase (placebo control) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo, significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement (REM) density compared with baseline. REM latency was not altered, however the first and second REM period interval were significantly shorter after tryptophan depletion. This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep.