Fear-enhanced visual search persists after amygdala lesions.
Ontology highlight
ABSTRACT:
SUBMITTER: Piech RM
PROVIDER: S-EPMC2949448 | biostudies-literature | 2010 Oct
REPOSITORIES: biostudies-literature
Publications
Fear-enhanced visual search persists after amygdala lesions.
Piech Richard M RM McHugo Maureen M Smith Stephen D SD Dukic Mildred S MS Van Der Meer Joost J Abou-Khalil Bassel B Zald David H DH
Neuropsychologia 20100714 12
Previous research has indicated that the amygdala is a critical neural substrate of the emotional modulation of attention. However, a recent case study suggests that the amygdala may not be essential for all types of emotion-attention interactions. In order to test this hypothesis, we assessed the visual-search performance of patients with unilateral amygdala lesions, matched controls, and medication-matched epilepsy patients with intact amygdalae. All participants completed a visual-search task ...[more]
Similar Datasets
Project description:People with autism spectrum disorders (ASD) have pervasive impairments in social interactions, a diagnostic component that may have its roots in atypical social motivation and attention. One of the brain structures implicated in the social abnormalities seen in ASD is the amygdala. To further characterize the impairment of people with ASD in social attention, and to explore the possible role of the amygdala, we employed a series of visual search tasks with both social (faces and people with different postures, emotions, ages, and genders) and non-social stimuli (e.g., electronics, food, and utensils). We first conducted trial-wise analyses of fixation properties and elucidated visual search mechanisms. We found that an attentional mechanism of initial orientation could explain the detection advantage of non-social targets. We then zoomed into fixation-wise analyses. We defined target-relevant effects as the difference in the percentage of fixations that fell on target-congruent vs. target-incongruent items in the array. In Experiment 1, we tested 8 high-functioning adults with ASD, 3 adults with focal bilateral amygdala lesions, and 19 controls. Controls rapidly oriented to target-congruent items and showed a strong and sustained preference for fixating them. Strikingly, people with ASD oriented significantly less and more slowly to target-congruent items, an attentional deficit especially with social targets. By contrast, patients with amygdala lesions performed indistinguishably from controls. In Experiment 2, we recruited a different sample of 13 people with ASD and 8 healthy controls, and tested them on the same search arrays but with all array items equalized for low-level saliency. The results replicated those of Experiment 1. In Experiment 3, we recruited 13 people with ASD, 8 healthy controls, 3 amygdala lesion patients and another group of 11 controls and tested them on a simpler array. Here our group effect for ASD strongly diminished and all four subject groups showed similar target-relevant effects. These findings argue for an attentional deficit in ASD that is disproportionate for social stimuli, cannot be explained by low-level visual properties of the stimuli, and is more severe with high-load top-down task demands. Furthermore, this deficit appears to be independent of the amygdala, and not evident from general social bias independent of the target-directed search.
| S-EPMC4317264 | biostudies-literature
Project description:Approach and avoidance constitute a basic dimension of all animal behavior. Although a large number of studies have investigated approach and avoidance elicited by specific sensory stimuli, comparatively little is known about default approach biases when stimulus information is absent or reduced. The amygdala is well known to contribute to approach and avoidance behaviors in response to specific sensory stimuli; we tested whether the amygdala's role might extend to situations in which stimulus information is reduced. In a novel task, 3 patients with rare bilateral amygdala lesions (and control subjects) made approach-related judgments about photos of intact faces and of the same faces with all internal facial features occluded. Direct comparisons of the judgments of these stimuli isolated a default bias. The patients showed a greater tendency than the control subjects to rate occluded faces as more approachable than whole faces. These findings suggest that the amygdala's role in approach behavior extends beyond responses to specific stimuli.
| S-EPMC4607547 | biostudies-literature
Project description:In addition to core symptoms, i.e., social interaction and communication difficulties and restricted and repetitive behaviors, autism is also characterized by aspects of superior perception. One well-replicated finding is that of superior performance in visual search tasks, in which participants have to indicate the presence of an odd-one-out element among a number of foils. Whether these aspects of superior perception contribute to the emergence of core autism symptoms remains debated. Perceptual and social interaction atypicalities could reflect co-expressed but biologically independent pathologies, as suggested by a "fractionable" phenotype model of autism. A developmental test of this hypothesis is now made possible by longitudinal cohorts of infants at high risk, such as of younger siblings of children with autism spectrum disorder (ASD). Around 20% of younger siblings are diagnosed with autism themselves, and up to another 30% manifest elevated levels of autism symptoms. We used eye tracking to measure spontaneous orienting to letter targets (O, S, V, and +) presented among distractors (the letter X; Figure 1). At 9 and 15 months, emerging autism symptoms were assessed using the Autism Observation Scale for Infants (AOSI;), and at 2 years of age, they were assessed using the Autism Diagnostic Observation Schedule (ADOS;). Enhanced visual search performance at 9 months predicted a higher level of autism symptoms at 15 months and at 2 years. Infant perceptual atypicalities are thus intrinsically linked to the emerging autism phenotype.
| S-EPMC4502951 | biostudies-literature
Project description:Posttraumatic stress disorder (PTSD) is both a prevalent and debilitating trauma-related disorder associated with dysregulated fear learning at the core of many of its signs and symptoms. Improvements in the currently available psychological and pharmacological treatments are needed in order to improve PTSD treatment outcomes and to prevent symptom relapse. In the present study, we used a putative animal model of PTSD that included presentation of immobilization stress (IMO) followed by fear conditioning (FC) a week later. We then investigated the acute effects of GR receptor activation on the extinction (EXT) of conditioned freezing, using dexamethasone administered systemically which is known to result in suppression of the HPA axis. In our previous work, IMO followed by tone-shock-mediated FC was associated with impaired fear EXT. In this study, we administered dexamethasone 4 h before EXT training and then examined EXT retention (RET) 24 h later to determine whether dexamethasone suppression rescued EXT deficits. Dexamethasone treatment produced dose-dependent enhancement of both EXT and RET. Dexamethasone was also associated with reduced amygdala Fkbp5 mRNA expression following EXT and after RET. Moreover, DNA methylation of the Fkbp5 gene occurred in a dose-dependent and time course-dependent manner within the amygdala. Additionally, we found dynamic changes in epigenetic regulation, including Dnmt and Tet gene pathways, as a function of both fear EXT and dexamethasone suppression of the HPA axis. Together, these data suggest that dexamethasone may serve to enhance EXT by altering Fkbp5-mediated glucocorticoid sensitivity via epigenetic regulation of Fkbp5 expression.
| S-EPMC4707829 | biostudies-literature
Project description:Neurons in the visual cortex quickly adapt to constant input, which should lead to perceptual fading within few tens of milliseconds. However, perceptual fading is rarely observed in everyday perception, possibly because eye movements refresh retinal input. Recently, it has been suggested that amplitudes of large saccadic eye movements are scaled to maximally decorrelate presaccadic and postsaccadic inputs and thus to annul perceptual fading. However, this argument builds on the assumption that adaptation within naturally brief fixation durations is strong enough to survive any visually disruptive saccade and affect perception. We tested this assumption by measuring the effect of luminance adaptation on postsaccadic contrast perception. We found that postsaccadic contrast perception was affected by presaccadic luminance adaptation during brief periods of fixation. This adaptation effect emerges within 100 milliseconds and persists over seconds. These results indicate that adaptation during natural fixation periods can affect perception even after visually disruptive saccades.
| S-EPMC8403744 | biostudies-literature
Project description:Auditory fear memory is thought to be maintained by fear conditioning-induced potentiation of synaptic efficacy, which involves enhanced expression of surface AMPA receptor (AMPAR) at excitatory synapses in the lateral amygdala (LA). Depotentiation, reversal of conditioning-induced potentiation, has been proposed as a cellular mechanism for fear extinction; however, a direct link between depotentiation and extinction has not yet been tested. To address this issue, we applied both ex vivo and in vivo approaches to rats in which fear memory had been consolidated. A unique form of depotentiation reversed conditioning-induced potentiation at thalamic input synapses onto the LA (T-LA synapses) ex vivo. Extinction returned the enhanced T-LA synaptic efficacy observed in conditioned rats to baseline and occluded the depotentiation. Consistently, extinction reversed conditioning-induced enhancement of surface expression of AMPAR subunits in LA synaptosomal preparations. A GluR2-derived peptide that blocks regulated AMPAR endocytosis inhibited depotentiation, and microinjection of a cell-permeable form of the peptide into the LA attenuated extinction. Our results are consistent with the use of depotentiation to weaken potentiated synaptic inputs onto the LA during extinction and provide strong evidence that AMPAR removal at excitatory synapses in the LA underlies extinction.
| S-EPMC2409248 | biostudies-literature
Project description:Previous literature demonstrated that the processing of emotional stimuli can interfere with goal-directed behavior. This has been shown primarily in the context of working memory tasks, but "emotional distraction" may affect also other processes, such as the orienting of visuo-spatial attention. During fMRI, we presented human subjects with emotional stimuli embedded within complex everyday life visual scenes. Emotional stimuli could be either the current target to be searched for or task-irrelevant distractors. Behavioral and eye-movement data revealed faster detection of emotional than neutral targets. Emotional distractors were found to be fixated later and for a shorter duration than emotional targets, suggesting efficient top-down control in avoiding emotional distraction. The fMRI data demonstrated that negative (but not positive) stimuli were mandatorily processed by limbic/para-limbic regions (namely, the right amygdala and the left insula), irrespective of current task relevance: that is, these regions activated for both emotional targets and distractors. However, analyses of inter-regional connectivity revealed a functional coupling between the left insula and the right prefrontal cortex that increased specifically during search in the presence of emotional distractors. This indicates that increased functional coupling between affective limbic/para-limbic regions and control regions in the frontal cortex can attenuate emotional distraction, permitting the allocation of spatial attentional resources toward task-relevant neutral targets in the presence of distracting emotional signals.
| S-EPMC6591190 | biostudies-literature
Project description:PurposeTo examine whether the age-related increase in visual field dependence persists in older adults with central field loss (CFL).MethodsTwenty individuals with CFL were grouped into participants with age-related binocular CFL (CFL, n = 9), age-related monocular CFL/relative scotomata (mCFL, n = 8), and CFL occurring at a young age (yCFL, n = 3). Seventeen controls were age-matched to the older CFL groups (OA) and three to the yCFL group (yOA). Participants judged the tilt direction of a rod presented at various orientations under conditions with and without a visual reference. Visual field dependence was determined as the difference in judgment bias between trials with and without the visual reference. Visual field dependence was examined between groups and relative to visual acuity and contrast sensitivity.ResultsAll older groups performed similarly without the visual reference. The CFL group showed greater visual field dependence than the OA group (Mann-Whitney U test; U = 39, P = 0.045). However, there was no group difference when considering all three older groups (Kruskal-Wallis ANOVA; H(2, N = 34) = 4.31, P = 0.116). Poorer contrast sensitivity correlated with greater visual field dependence (P = 0.017; ρ = -0.43).ConclusionsVisual field dependence persists in older adults with CFL and seems exacerbated in those with dense binocular scotomata. This could be attributed to the sensitivity of the spared peripheral retina to orientation and motion cues. The relationship with contrast sensitivity further suggests that a decline in visual function is associated with an increase in visual field dependence beyond the effects of normal aging. These observations can guide tailored care and rehabilitation in older adults with CFL.
| S-EPMC10866173 | biostudies-literature
Project description:The central amygdala (Ce), particularly its medial sector (CeM), is the main output station of the amygdala for conditioned fear responses. However, there is uncertainty regarding the nature of CeM control over conditioned fear. The present study aimed to clarify this question using unit recordings in rats. Fear conditioning caused most CeM neurons to increase their conditioned stimulus (CS) responsiveness. The next day, CeM cells responded similarly during the recall test, but these responses disappeared as extinction of conditioned fear progressed. In contrast, the CS elicited no significant average change in central lateral (CeL) firing rates during fear conditioning and a small but significant reduction during the recall test. Yet, cell-by-cell analyses disclosed large but heterogeneous CS-evoked responses in CeL. By the end of fear conditioning, roughly equal proportions of CeL cells exhibited excitatory (CeL(+)) or inhibitory (CeL(-)) CS-evoked responses (?10%). The next day, the proportion of CeL(-) cells tripled with no change in the incidence of CeL(+) cells, suggesting that conditioning leads to overnight synaptic plasticity in an inhibitory input to CeL(-) cells. As in CeM, extinction training caused the disappearance of CS-evoked activity in CeL. Overall, these findings suggest that conditioned freezing depends on increased CeM responses to the CS. The large increase in the incidence of CeL(-) but not CeL(+) cells from conditioning to recall leads us to propose a model of fear conditioning involving the potentiation of an extrinsic inhibitory input (from the amygdala or elsewhere) to CeL, ultimately leading to disinhibition of CeM neurons.
| S-EPMC3080118 | biostudies-literature
Project description:Multiple sclerosis (MS) lesions demonstrate immunopathological heterogeneity in patterns of demyelination. Previous cross-sectional studies reported immunopatterns of demyelination were identical among multiple active demyelinating lesions from the same individual, but differed between individuals, leading to the hypothesis of intraindividual pathological homogeneity and interindividual heterogeneity. Other groups suggested a time-dependent heterogeneity of lesions. The objective of our present study was to analyze tissue samples collected longitudinally to determine whether patterns of demyelination persist over time within a given patient.Archival tissue samples derived from patients with pathologically confirmed central nervous system inflammatory demyelinating disease who had undergone either diagnostic serial biopsy or biopsy followed by autopsy were analyzed immunohistochemically. The inclusion criteria consisted of the presence of early active demyelinating lesions--required for immunopattern classification--obtained from the same patient at 2 or more time points.Among 1,321 surgical biopsies consistent with MS, 22 cases met the study inclusion criteria. Twenty-one patients (95%) showed a persistence of immunopathological patterns in tissue sampled from different time points. This persistence was demonstrated for all major patterns of demyelination. A single patient showed features suggestive of both pattern II and pattern III on biopsy, but only pattern II among all active lesions examined at autopsy.These findings continue to support the concept of patient-dependent immunopathological heterogeneity in early MS and suggest that the mechanisms and targets of tissue injury may differ among patient subgroups. These observations have potentially significant implications for individualized therapeutic approaches.
| S-EPMC4070313 | biostudies-literature