Manipulating affective state influences conditioned appetitive responses

Affective states influence how individuals process information and behave. Some theories predict emotional congruency effects (e.g. preferential processing of negative information in negative affective states). Emotional congruency should theoretically obstruct the learning of reward associations (appetitive learning) and their ability to guide behaviour under negative mood. Two studies tested the effects of the induction of a negative affective state on appetitive Pavlovian learning, in which neutral stimuli were associated with chocolate (Experiment 1) or alcohol (Experiment 2) rewards. In both experiments, participants showed enhanced approach tendencies towards predictors of reward after a negative relative to a positive performance feedback manipulation. This increase was related to a reduction in positive affect in Experiment 1 only. No effects of the manipulation on conditioned reward expectancies, craving, or consumption were observed. Overall, our findings support the idea of counter-regulation, rather than emotional congruency effects. Negative affective states might therefore serve as a vulnerability factor for addiction, through increasing conditioned approach tendencies.     

Mechanisms underlying speech sound discrimination and categorization in humans and zebra finches

Speech sound categorization in birds seems in many ways comparable to that by humans, but it is unclear what mechanisms underlie such categorization. To examine this, we trained zebra finches and humans to discriminate two pairs of edited speech sounds that varied either along one dimension (vowel or speaker sex) or along two dimensions (vowel and speaker sex). Sounds could be memorized individually or categorized based on one dimension or by integrating or combining both dimensions. Once training was completed, we tested generalization to new speech sounds that were either more extreme, more ambiguous (i.e., close to the category boundary), or within-category intermediate between the trained sounds. Both humans and zebra finches learned the one-dimensional stimulus–response mappings faster than the two-dimensional mappings. Humans performed higher on the trained, extreme and within-category intermediate test-sounds than on the ambiguous ones. Some individual birds also did so, but most performed higher on the trained exemplars than on the extreme, within-category intermediate and ambiguous test-sounds. These results suggest that humans rely on rule learning to form categories and show poor performance when they cannot apply a rule. Birds rely mostly on exemplar-based memory with weak evidence for rule learning.     

Selective Attention and Anxiety: A Perspective on Developmental Issues and the Causal Status

A plethora of studies on selective information processing in anxiety have been carried out over the past two decades. One of the most robust findings is that anxiety is associated with selective attention (SA) for threatening information. The rationale of research into SA is that it is assumed to play a vital role in the maintenance, and even in the etiology of anxiety disorders. It is the aim of this paper to explicate on the validity of this assumption. There is ample evidence that anxiety enhances SA. Although there is a lack of studies on the effect of SA on anxiety, there is now some evidence that SA increases the level of anxiety. This leads us to conclude that SA is not a by-product of anxiety only. Hence, the suggestion that SA plays a role in the maintenance of anxiety disorders seems to be justified. Studies on SA in children suggest that if SA plays any role at all in the development of anxiety disorders, it is not the SA in itself that is a vulnerability factor, but the continuation of this SA. Individuals who develop an anxiety disorder could have difficulty learning to inhibit this SA. Considering the finding that SA increases the level of anxiety, the authors suggest that anxiety in childhood causes failure to inhibit SA, which in turn enhances the vulnerability to anxiety disorder in adulthood.     

Disrupting reconsolidation: pharmacological and behavioral manipulations

We previously demonstrated that disrupting reconsolidation by pharmacological manipulations "deleted" the emotional expression of a fear memory in humans. If we are to target reconsolidation in patients with anxiety disorders, the disruption of reconsolidation should produce content-limited modifications. At the same time, the fear-erasing effects should not be restricted to the feared cue itself considering that fear generalization is a main characteristic of anxiety disorders. In Experiment I and Experiment I(b), we addressed these issues using a within-subject differential startle fear conditioning paradigm and a test of fear generalization. In Experiment II, we tested whether a behavioral approach targeting the reconsolidation through extinction learning was also effective in weakening the original fear memory. A behavioral procedure is evidently preferred over drug manipulations provided that similar effects can be obtained. Here, the extinction procedure subsequent to retrieval did not "erase" the emotional expression of the fear memory as the retrieval techniques (i.e., reminder shocks and reacquisition) unveiled a return of the startle fear response to the fear-relevant stimuli. In contrast, β-adrenergic receptor blockade during reconsolidation selectively deleted the fear-arousing aspects of the memory (i.e., startle fear response) along with its category-related information. The pharmacological manipulation rendered the core memory trace too weak to observe fear generalization after successful reacquisition. Hence, relearning following the disruption of reconsolidation seems to be qualitatively different from initial learning. Our findings demonstrate that disrupting reconsolidation by pharmacological manipulations, although selective, undermines the generalization of fear, a key feature of anxiety disorders.     

Noradrenergic enhancement of associative fear memory in humans

Ample evidence in animals and humans supports the noradrenergic modulation in the formation of emotional memory. However, in humans the effects of stress on emotional memory are traditionally investigated by declarative memory tests (e.g., recall, recognition) for non-associative emotional stimuli (e.g., stories, pictures). Given that anxiety disorders are thought to originate from associative learning processes and are characterized by distressing emotional responses, the existing literature seems to be inconclusive for the understanding of these disorders. Here, we tested whether noradrenaline strengthens the emotional expression of associative fear memory by using a differential fear conditioning procedure in humans. Stimulation of the noradrenergic system by the administration of yohimbine HCl (20 mg) during memory formation did not directly augment the differential startle fear response 48 h later. Yet, the other retention tests uncovered that the administration of yohimbine HCl contrary to placebo pill extensively delayed the process of extinction learning and generated a superior recovery of fear (i.e., reinstatement and reacquisition). Conversely, the yohimbine HCl manipulation did not affect the skin conductance responding and the US expectancy ratings, emphasizing the concept of multiple memory systems. To our knowledge this is the first demonstration in humans that increased noradrenaline release during or shortly after a stressful event strengthens the formation of associative fear memory traces. The present findings suggest that noradrenaline may play an important role in the etiology and maintenance of anxiety disorders.     

Neural substrates of individual differences in human fear learning: Evidence from concurrent fMRI, fear-potentiated startle, and US-expectancy data

To provide insight into individual differences in fear learning, we examined the emotional and cognitive expressions of discriminative fear conditioning in direct relation to its neural substrates. Contrary to previous behavioral-neural (fMRI) research on fear learning--in which the emotional expression of fear was generally indexed by skin conductance--we used fear-potentiated startle, a more reliable and specific index of fear. While we obtained concurrent fear-potentiated startle, neuroimaging (fMRI), and US-expectancy data, healthy participants underwent a fear-conditioning paradigm in which one of two conditioned stimuli (CS(+) but not CS(-)) was paired with a shock (unconditioned stimulus [US]). Fear learning was evident from the differential expressions of fear (CS(+) > CS(-)) at both the behavioral level (startle potentiation and US expectancy) and the neural level (in amygdala, anterior cingulate cortex, hippocampus, and insula). We examined individual differences in discriminative fear conditioning by classifying participants (as conditionable vs. unconditionable) according to whether they showed successful differential startle potentiation. This revealed that the individual differences in the emotional expression of discriminative fear learning (startle potentiation) were reflected in differential amygdala activation, regardless of the cognitive expression of fear learning (CS-US contingency or hippocampal activation). Our study provides the first evidence for the potential of examining startle potentiation in concurrent fMRI research on fear learning.     

The utility of screen for child anxiety related emotional disorders (scared) as a tool for identifying children at high risk for prevalent anxiety disorders

Abstract

The current study examined the utility of the Screen for Child Anxiety Related Emotional Disorders (SCARED) as a screening tool for the identification of children at high risk for prevalent childhood anxiety disorders. The child version of the Structured Clinical Interview for DSM (KSCID) was used as the diagnostic standard. It was investigated whether SCARED scores are indicative for the presence of generalized anxiety disorder, separation anxiety disorder, and social phobia. Five-hundred-and-thirty-seven children aged 7–14 years completed the SCARED. From this sample, 82 children were selected on the basis of their SCARED scores. A subgroup of these children scored relatively high on the generalized anxiety disorder, separation anxiety disorder, and/or social phobia scale(s) of the SCARED. A comparison group of children scored relatively low on these SCARED scales. Both groups of children then received the semi-structured interview to assess to what extent they fulfilled the DSM-IV criteria for the relevant anxiety disorders. Results provided some support for the predictive validity of the SCARED generalized anxiety disorder and separation anxiety disorder subscales. The implications of these findings for the detection of anxiety disorders in normal children are briefly discussed.     

Peritraumatic dissociation and posttraumatic stress after pregnancy loss: a prospective study

This study examined (1). predictors for peritraumatic dissociation, (2). its relations with acute and chronic symptoms of posttraumatic stress disorder (PTSD), and (3). pathways regarding these relations in response to pregnancy loss. In early pregnancy, about 1370 women volunteers completed questionnaires for neuroticism, control over emotions, dissociative tendencies, absorption, and prior life events. Of these, 126 subsequently experienced pregnancy loss and most of them completed measures 1 month (N = 118) and 4 months (N = 104) later. At 1 month, peritraumatic dissociation, memory of pregnancy loss (degree of fragmentation, sensory impressions, and emotional intensity), thought suppression, and PTSD symptoms were assessed, and at 4 months, PTSD symptoms were re-assessed. Peritraumatic dissociation was predicted by prior low control over emotions, dissociative tendencies, and lower education. It was not predicted by neuroticism, absorption, and prior life events. Peritraumatic dissociation was related to acute PTSD symptoms and LISREL analyses indicated that self-reported memory fragmentation and thought suppression of pregnancy loss mediated this relation. It also predicted chronic PTSD symptoms, and this relation was mediated by acute PTSD symptoms.     

Fearing shades of grey: individual differences in fear responding towards generalisation stimuli

Individual differences in fear generalisation have been proposed to play a role in the aetiology and/or maintenance of anxiety disorders, but few data are available to directly support that claim. The research that is available has focused mostly on generalisation of peripheral and central physiological fear responses. Far less is known about the generalisation of avoidance, the behavioural component of fear. In two experiments, we evaluated how neuroticism, a known vulnerability factor for anxiety, modulates an array of fear responses, including avoidance tendencies, towards generalisation stimuli (GS). Participants underwent differential fear conditioning, in which one conditioned stimulus (CS+) was repeatedly paired with an aversive outcome (shock; unconditioned stimulus, US), whereas another was not (CS?). Fear generalisation was observed across measures in Experiment 1 (US expectancy and evaluative ratings) and Experiment 2 (US expectancy, evaluative ratings, skin conductance, startle responses, safety behaviours), with overall highest responding to the CS+, lowest to the CS? and intermediate responding to the GSs. Neuroticism had very little impact on fear generalisation (but did affect GS recognition rates in Experiment 1), in line with the idea that fear generalisation is largely an adaptive process.