Overgeneralization Of Fear Research Articles

Sex differences in auditory fear discrimination are associated with altered medial prefrontal cortex function

The increased prevalence of post-traumatic stress disorder (PTSD) that is observed in women may involve sex differences in learned fear inhibition and medial prefrontal cortex (mPFC) function. PTSD is characterized by fear overgeneralization involving impaired fear regulation by safety signals. We recently found that males show fear discrimination and females show fear generalization involving reduced safety signalling after extended fear discrimination training. Here we determined if these sex differences involve altered mPFC function. Male and female rats underwent three days of auditory fear discrimination training, where one tone (CS+) was paired with footshock and another tone (CS−) was presented alone. Local field potentials were recorded from prelimbic (PL) and infralimbic (IL) mPFC during retrieval. We found that males discriminated and females generalized based on cue-induced freezing at retrieval. This was accompanied by sex differences in basal theta and gamma oscillations in PL and IL. Importantly, males also showed PL/IL theta activation during safety signalling by the CS− and IL gamma activation in response to the threat-related CS+, both of which were absent in females. These results add to growing evidence indicating that sex differences in learned fear inhibition are associated with altered mPFC function.

Individual differences in human fear generalization\u2014pattern identification and implications for anxiety disorders

Previous research indicates that anxiety disorders are characterized by an overgeneralization of conditioned fear as compared with healthy participants. Therefore, fear generalization is considered a key mechanism for the development of anxiety disorders. However, systematic investigations on the variance in fear generalization are lacking. Therefore, the current study aims at identifying distinctive phenotypes of fear generalization among healthy participants. To this end, 1175 participants completed a differential fear conditioning phase followed by a generalization test. To identify patterns of fear generalization, we used a k-means clustering algorithm based on individual arousal generalization gradients. Subsequently, we examined the reliability and validity of the clusters and phenotypical differences between subgroups on the basis of psychometric data and markers of fear expression. Cluster analysis reliably revealed five clusters that systematically differed in mean responses, differentiation between conditioned threat and safety, and linearity of the generalization gradients, though mean response levels accounted for most variance. Remarkably, the patterns of mean responses were already evident during fear acquisition and corresponded most closely to psychometric measures of anxiety traits. The identified clusters reliably described subgroups of healthy individuals with distinct response characteristics in a fear generalization test. Following a dimensional view of psychopathology, these clusters likely delineate risk factors for anxiety disorders. As crucial group characteristics were already evident during fear acquisition, our results emphasize the importance of average fear responses and differentiation between conditioned threat and safety as risk factors for anxiety disorders.

Role of the dorsal periaqueductal gray in posttraumatic stress disorder: mediation by dopamine and neurokinin

In susceptible individuals, exposure to intensely traumatic life events can lead to the development of posttraumatic stress disorder (PTSD), including long-term dysregulation of the contextual processing of aversive stimuli, the overgeneralization of learned fear, and impairments in the ability to learn or respond to safety signals. The neuropathophysiological changes that underlie PTSD remain incompletely understood. Attention has focused on forebrain structures associated with fear processing. Here we consider evidence from human and animal studies that long-lasting changes in functional connectivity between the midbrain periaqueductal gray (dPAG) and amygdala may be one of the precipitating events that contribute to PTSD. Long-lasting neuroplastic changes in the dPAG can persist after a single aversive stimulation and are pharmacologically labile. The early stage (at least up to 24 h post-stimulation) involves neurokinin-1 receptor-mediated events in the PAG and amygdala and is also regulated by dopamine, both of which are mainly involved in transferring ascending aversive information from the dPAG to higher brain structures, mainly the amygdala. Changes in the functional connectivity within the dPAG-amygdala circuit have been reported in PTSD patients. We suggest that further investigations of plasticity and pharmacology of the PAG-amygdala network provide a promising target for understanding pathophysiological circuitry that underlies PTSD in humans and that dopaminergic and neurokininergic drugs may have a potential for the treatment of psychiatric disorders that are associated with a dysfunctional dPAG.

Reducing avoidance in adults with high spider fear using perceptual discrimination training.

Fear overgeneralization is a central feature of anxiety disorders and can lead to excessive avoidance. As perceptual discrimination is a key component of fear overgeneralization, a perceptual discrimination training task was created aimed at improving perceptual discrimination and reducing fear overgeneralization. Participants with high spider fear were randomized into training or placebo conditions. After completing their assigned task, perceptual discrimination was tested. Thereafter, participants completed a behavioral avoidance test, consisting of five stimuli ranging from a paper spider to a live tarantula. Last, participants completed a threat/safety discrimination task using schematic morphs ranging from a flower to a spider, while self-report and skin conductance responses were collected. The training group showed better perceptual discrimination during the test than did the placebo group. Furthermore, as stimuli became increasingly similar to a live spider, participants in the training group exhibited decreased avoidance behavior. Finally, participants in the training group indicated that schematic morphs were less similar to a spider and showed less physiological arousal than did the placebo group. Together, these results attest to the possible clinical relevance of the perceptual discrimination training.

Anterior Cingulate Cortex and Ventral Hippocampal Inputs to the Basolateral Amygdala Selectively Control Generalized Fear.

A common symptom of anxiety disorders is the overgeneralization of fear across a broad range of contextual cues. We previously found that the ACC and ventral hippocampus (vHPC) regulate generalized fear. Here, we investigate the functional projections from the ACC and vHPC to the amygdala and their role in governing generalized fear in a preclinical rodent model. A chemogenetic approach (designer receptor exclusively activated by designer drugs) was used to inhibit glutamatergic projections from the ACC or vHPC that terminate within the BLA at recent (1 d) or remote (28 d) time points after contextually fear conditioning male mice. Inactivating ACC or vHPC projections to the BLA significantly reduced generalized fear to a novel, nonthreatening context but had no effect on fear to the training context. Further, our data indicate that the ACC-BLA circuit supports generalization in a time-independent manner. We also identified, for the first time, a strictly time-dependent role of the vHPC-BLA circuit in supporting remote generalized contextual fear. Dysfunctional signaling to the amygdala from the ACC or the HPC could underlie overgeneralized fear responses that are associated with anxiety disorders. Our findings demonstrate that the ACC and vHPC regulate fear expressed in novel, nonthreatening environments via projections to the BLA but do so as a result of training intensity or time, respectively.SIGNIFICANCE STATEMENT Anxiety disorders are characterized by a common symptom that promotes overgeneralization of fear in nonthreatening environments. Dysregulation of the amygdala, ACC, or hippocampus (HPC) has been hypothesized to contribute to increased fear associated with anxiety disorders. Our findings show that the ACC and HPC projections to the BLA regulate generalized fear in nonthreatening, environments. However, descending ACC projections control fear generalization independent of time, whereas HPC projections play a strictly time-dependent role in regulating generalized fear. Thus, dysfunctional ACC/HPC signaling to the BLA may be a predominant underlying mechanism of nonspecific fear associated with anxiety disorders. Our data have important implications for predictions made by theories about aging memories and interactions between the HPC and cortical regions.

Anterior Cingulate Cortex to Ventral Hippocampus Circuit Mediates Contextual Fear Generalization.

Contextual fear memory becomes less context-specific over time, a phenomenon referred to as contextual fear generalization. Overgeneralization of contextual fear memory is a core symptom of post-traumatic stress disorder (PTSD), but circuit mechanisms underlying the generalization remain unclear. We show here that neural projections from the anterior cingulate cortex (ACC) to ventral hippocampus (vHPC) mediate contextual fear generalization in male mice. Retrieval of contextual fear in a novel context at a remote time point activated cells in the ACC and vHPC, as indicated by significantly increased C-fos+ cells. Using chemogenetic or photogenetic manipulations, we observed that silencing the activity of ACC or vHPC neurons reduced contextual fear generalization at the remote time point, whereas stimulating the activity of ACC or vHPC neurons facilitated contextual fear generalization at a recent time point. We found that ACC neurons projected to the vHPC unidirectionally, and importantly, silencing the activity of projection fibers from the ACC to vHPC inhibited contextual fear generalization at the remote time point. Together, our findings reveal an ACC to vHPC circuit that controls expression of fear generalization and may offer new strategies to prevent or reverse contextual fear generalization in subjects with anxiety disorders, especially in PTSD.SIGNIFICANCE STATEMENT Overgeneralization of contextual fear memory is a cardinal feature of PTSD, but circuit mechanisms underlying it remain unclear. Our study indicates that neural projections from the anterior cingulate cortex to ventral hippocampus control the expression of contextual fear generalization. Thus, manipulating the circuit may prevent or reverse fear overgeneralization in subjects with PTSD.

T18. Trait Anxiety Associated With Differences in BOLD Activation During Fear Generalization Task

Pathological anxiety has been associated with overgeneralization of conditioned fear, wherein safe stimuli are perceived as threatening due to perceptual similarity to a threat. Neuroimaging studies have implicated structures, including the insula, hippocampus, ventromedial prefrontal cortex, and precuneus, to be sensitive to stimulus differentiation.

The effect of transcutaneous vagus nerve stimulation on fear generalization and subsequent fear extinction.

Fear overgeneralization is thought to be one of the cardinal processes underlying anxiety disorders, and a determinant of the onset, maintenance and recurrence of these disorders. Animal studies have shown that stimulating the vagus nerve (VNS) affects neuronal pathways implicated in pattern separation and completion, suggesting it may reduce the generalization of a fear memory to novel situations. In a one-day study, 58 healthy students were subjected to a fear conditioning, fear generalization, and fear extinction paradigm. Participants were randomly assigned to receive either transcutaneous auricular VNS (tVNS; final N = 29) or sham stimulation (final N = 29) during the generalization and extinction phases. tVNS did not affect fear generalization, as reflected by US expectancy ratings and fear potentiated startle responses. However, participants who received tVNS reported lower US expectancy ratings to the CS+ during the extinction phase, possibly reflecting a stronger declarative extinction of fear. No effects of tVNS on fear potentiated startle responses during extinction were found. The pattern of findings regarding extinction of declarative fear suggest a facilitating effect of tVNS.

Sex Differences in Remote Contextual Fear Generalization in Mice.

The generalization of fear is adaptive in that it allows an animal to respond appropriately to novel threats that are not identical to previous experiences. In contrast, the overgeneralization of fear is maladaptive and is a hallmark of post-traumatic stress disorder (PTSD), a psychiatric illness that is characterized by chronic symptomatology and a higher incidence in women compared to men. Therefore, understanding the neural basis of fear generalization at remote time-points in female animals is of particular translational relevance. However, our understanding of the neurobiology of fear generalization is largely restricted to studies employing male mice and focusing on recent time-points (i.e., within 24–48 h following conditioning). To address these limitations, we examined how male and female mice generalize contextual fear at remote time intervals (i.e., 3 weeks after conditioning). In agreement with earlier studies of fear generalization at proximal time-points, we find that the test order of training and generalization contexts is a critical determinant of generalization and context discrimination, particularly for female mice. However, tactile elements that are present during fear conditioning are more salient for male mice. Our study highlights long-term sex differences in defensive behavior between male and female mice and may provide insight into sex differences in the processing and retrieval of remote fear memory observed in humans.

Reducing fear overgeneralization in children using a novel perceptual discrimination task

Fear generalization, while adaptive, can be detrimental when occurring in excess. To this end a perceptual discrimination training task was created with a goal of decreasing fear overgeneralization. The current study tested the effectiveness of the training task among typically-developing children.Participants (n = 73) were randomly assigned into a training, placebo or no task group. Following a differential fear-conditioning task, participants in the first two groups underwent the discrimination training or placebo task. An assessment task was then administered. Finally, all participants completed a fear generalization test, consisting of 11 morphs ranging in perceptual similarity from the threat cue to the safety cue. Physiological and self-report measures were collected.Fear-conditioning was achieved in both physiological and self-report measures. Further, in the assessment task, the training group showed better perceptual discrimination than did the placebo group. Last, the training group exhibited less overgeneralization of affective stimuli as indicated by a physiological measure than did the two control conditions.Findings suggest that the perceptual discrimination training task effectively moderated fear overgeneralization in children. This adds to previous evidence of the task's effectiveness among adults.

Chronic fluoxetine prevents fear memory generalization and enhances subsequent extinction by remodeling hippocampal dendritic spines and slowing down systems consolidation

Fear memory overgeneralization contributes to the genesis and persistence of anxiety disorders and is a central hallmark in the pathophysiology of post-traumatic stress disorder (PTSD). Recent findings suggest that fear generalization is closely related to hippocampal dependency during retrieval. The selective serotonin reuptake inhibitor (SSRI) fluoxetine has been used as a first-line treatment for PTSD; however, how it exerts its therapeutic effect remains a matter of debate. Here, using contextual fear conditioning in rats, we show that chronic fluoxetine treatment prevents fear generalization and enhances subsequent extinction. Moreover, fluoxetine treatment after extinction prevents spontaneous recovery. The mechanism through which fluoxetine affects generalization and extinction seems to be through the postponement of systems consolidation, thereby maintaining hippocampal involvement during retrieval. Such an effect relies on a remodeling of dendritic spines in the hippocampus, as well as the number of mature, mushroom-type spines promoted by fluoxetine treatment. In order to further investigate whether fear generalization is a potential predictor of extinction effectiveness, we categorized a large naive population according to their generalization rate. We found that discriminator rats showed a better extinction profile compared to generalizers, suggesting that the generalization rate predicts extinction effectiveness. Hence, we propose that the therapeutic strategy of choice should take into account the extension of memory generalization, in which therapies based on extinction could induce a better outcome in patients who present less fear overgeneralization. These results open new avenues for the development of interventions that prevent fear generalization by maintaining memory dependency of the hippocampus.

No Time-Dependent Effects of Psychosocial Stress on Fear Contextualization and Generalization: A Randomized-Controlled Study With Healthy Participants

The formation of context-dependent fear memories (fear contextualization) can aid the recognition of danger in new, similar, situations. Overgeneralization of fear is often seen as hallmark of anxiety and trauma-related disorders. In this randomized-controlled study, we investigated whether exposure to a psychosocial stressor influences retention of fear contextualization and generalization in a time-dependent manner. The Trier Social Stress Test was used to induce psychosocial stress. Healthy male participants (n = 117) were randomly divided into three experimental groups that were subjected to the acquisition phase of the Fear Generalization Task: (1) without stress, (2) immediately after acute stress, or (3) 2 h after acute stress. In this task, a male with neutral facial expression (conditioned stimuli) was depicted in two different contexts that modulated the conditioned stimuli–unconditioned stimuli (=shock) association (threat, safe). Salivary alpha-amylase and cortisol levels were measured throughout the experiment. After a 24-h delay, context-dependency of fear memory was investigated with an unannounced memory test consisting of the threat and safe contexts alternated with a novel context (the generalization context). Multilevel analyses revealed that participants showed increased fear-potentiated startle responses to the conditioned stimuli in the threat compared to the safe context, at the end of the acquisition phase, indicating adequate fear contextualization. Directly after acquisition, there were no time-dependent effects of psychosocial stress on fear contextualization. Context-dependency of fear memories was retained 24 h later, as fear-potentiated startle responding was modulated by context (threat > safe or novel). At that time, the context-dependency of fear memories was also not influenced by the early or late effects of the endogenous stress response during acquisition. These results with experimental stress deviate in some aspects from those earlier obtained with exogenous hydrocortisone administration, suggesting a distinct role for stress mediators other than cortisol.

Problematic attention processing and fear learning in adolescent anxiety: Testing a combined cognitive and learning processes model

Background and objectivesAnxiety in adolescence is characterised by disturbances in attentional processes and the overgeneralisation of fear, however, little is known about the combined and reciprocal effects of and between these factors on youth anxiety. The present study investigated whether attention (attention allocation and control) and fear generalisation processes together predict more variance on adolescent anxiety symptoms than each factor in isolation, and explored their interrelations. Methods197 adolescents completed a novel conditioning task, which paired balloon cues with mildly aversive or neutral outcomes. A spatial cueing task, and self-report measures of emotional attentional control and anxiety, were also completed. ResultsThreat-avoidant attention allocation biases, impaired attention control, and exaggerated fear generalisation together predicted greater variance in anxiety symptoms (55.3%), than each set of fear and attention processes in isolation. Results also provided evidence of an interplay between these factors. Individual differences in threat-avoidant attention allocation biases predicted variability in the generalisation of fear, whilst the association between heightened anxiety and the overgeneralization of fear was moderated by poor attention control. ConclusionsThis study provides unique evidence of the combined effects of attention and fear generalisation mechanisms in explaining youth anxiety, and interrelations between these factors. Importantly, results suggested that deficiencies in attention control may bring out anxiety-associated impairments in fear generalisation. LimitationsWe relied on self-reported ratings of fear during generalization and also of attention control. Thus demand effects cannot be discounted. Reaction-time measures of attention focus are also indirect assessments of attention that may lack precision.

Trauma exposure acutely alters neural function during Pavlovian fear conditioning

Posttraumatic stress disorder (PTSD) is associated with dysfunction of the neural circuitry that supports fear learning and memory processes. However, much of what is known about neural dysfunction in PTSD is based on research in chronic PTSD populations. Less is known about neural function that supports fear learning acutely following trauma exposure. Determining the acute effects of trauma exposure on brain function would provide new insight into the neural processes that mediate the cognitive-affective dysfunction associated with PTSD. Therefore, the present study investigated neural activity that supports fear learning and memory processes in recently Trauma-Exposed (TE) and Non-Trauma-Exposed (NTE) participants. Participants completed a Pavlovian fear conditioning procedure during functional magnetic resonance imaging (fMRI). During fMRI, participants’ threat expectancy was continuously monitored. NTE participants showed greater threat expectancy during warning than safety cues, while no difference was observed in the TE group. This finding suggests TE participants overgeneralized the fear association to the safety cue. Further, only the TE group showed a negative relationship between fMRI signal responses within dorsomedial prefrontal cortex (PFC) and threat expectancy during safety cues. These results suggest the dorsomedial PFC mediates overgeneralization of learned fear as an acute result of trauma exposure. Finally, neural activity within the PFC and inferior parietal lobule showed a negative relationship with PTSD symptom severity assessed three months posttrauma. Thus, neural activity measured acutely following trauma exposure predicted future PTSD symptom severity. The present findings elucidate the acute effects of trauma exposure on cognitive-affective function and provide new insight into the neural mechanisms of PTSD.

Dentate granule cell recruitment of feedforward inhibition governs engram maintenance and remote memory generalization

Memories become less precise and generalize over time as memory traces re-organize in hippocampal-cortical networks. Increased time-dependent loss of memory precision characterizes overgeneralization of fear in post-traumatic stress disorder (PTSD) and age-related cognitive impairments. In the hippocampal dentate gyrus (DG), memories are thought to be encoded by so-called “engram-bearing” dentate granule cells (eDGCs). Here we show using rodents that contextual fear conditioning increases connectivity between eDGCs and inhibitory interneurons in the downstream hippocampal CA3 region. We identify actin-binding LIM protein 3 (abLIM3) as a mossy fiber terminal localized cytoskeletal factor, whose levels decrease upon learning. Downregulation of abLIM3 in DGCs was sufficient to increase connectivity with CA3 stratum lucidum interneurons (SLINs), promote parvalbumin (PV) SLIN activation, enhance feed-forward inhibition onto CA3, and maintain a fear memory engram in the dentate gyrus (DG) over time. Furthermore, abLIM3 downregulation in DGCs conferred conditioned context-specific reactivation of memory traces in hippocampal-cortical and amygdalar networks and decreased fear memory generalization at remote time points. Consistent with age-related hyperactivity of CA3, learning failed to increase DGC-SLIN connectivity in 17 month-old mice, whereas abLIM3 downregulation was sufficient to restore DGC-SLIN connectivity, increase PV-SLIN activation and improve remote memory precision. These studies exemplify a connectivity-based strategy targeting a molecular brake of feedforward inhibition in DG-CA3 that may be harnessed to decrease time-dependent memory generalization in PTSD and improve memory precision in aging.

Generalization of Conscious Fear Is Positively Correlated with Anxiety, but Not with Depression.

Generalization of learned fear has been considered to be critical for our survival. Patients with anxiety problems show overgeneralization of learned fear, as reflected by defensive physiological responses to harmless stimuli. Together with these physiological responses, conscious feeling of fear is a seminal part of emotional process that is directly related to the suffering of anxiety patients. However, the effect of anxiety on the generalization of conscious feeling remains unclear. We thus focused on the question whether the generalization of conscious feeling of fear depends on individual anxiety level in nonpatient participants. To address this question, we developed a fear generalization paradigm using natural scene images. We found that subjective feeling of fear was generalized to similar stimuli with the conditioned stimuli (CS), and that this generalization of conscious fear was positively correlated with the level of individual anxiety. Anxiety and depression frequently co-occur, but the individual depression level was not correlated with the fear generalization. These suggest that individual anxiety level mainly affects the generalization of conscious fear.

Stress promotes generalization of older but not recent threat memories

Stress broadly affects the ability to regulate emotions and may contribute to generalization of threat-related behaviors to harmless stimuli. Behavioral generalization also tends to increase over time as memory precision for recent events gives way to more gist-like representations. Thus, acute stress coupled with a delay in time from a negative experience may be a strong predictor of the transition from normal to generalized fear expression. Here, we investigated the effect of a single-episode acute stressor on generalization of aversive learning when stress is administered either immediately after an aversive learning event or following a delay. In a between-subjects design, healthy adult volunteers underwent threat (fear) conditioning using a tone-conditioned stimulus paired with an electric shock to the wrist and another tone not paired with shock. Behavioral generalization was tested to a range of novel tones either on the same day (experiment 1) or 24 h later (experiment 2) and was preceded by either an acute stress induction or a control task. Anticipatory sympathetic arousal [i.e., skin conductance responses (SCRs)] and explicit measures of shock expectancy served as dependent measures. Stress administered shortly after threat conditioning did not affect behavioral generalization. In contrast, stress administered following a delay led to heightened arousal and increased generalization of SCRs and explicit measures of shock expectancy. These findings show that acute stress increases generalization of older but not recent threat memories and have clinical relevance to understanding overgeneralization characteristics of anxiety and stress-related disorders.

Distraction/Suppression and Distress Endurance diminish the extent to which generalized conditioned fear is associated with maladaptive behavioral avoidance

A central conditioning correlate of clinical anxiety is the over-generalization of Pavlovian fear to safe stimuli resembling conditioned danger cues (CS+). Though much of the pathogenic influence of such generalization may lie in the unnecessary behavioral avoidance it evokes, few studies have examined maladaptive avoidance associated with Pavlovian generalization. Lab-based assessments of this process, here referred to as instrumental avoidance from Pavlovian generalization (IAP-G), have recently begun. The current study represents a next step in this line of work by examining personality factors that may reduce maladaptive IAP-G. This is a clinically relevant effort, as such traits may reflect resilience factors, with high levels reducing the likelihood of maladaptive generalized avoidance following Pavlovian generalization. Here we focus on the effects of Distraction/Suppression (DS) and Distress Endurance (DE) on IAP-G. Results indicate that both DS and DE moderate IAP-G by weakening relations between Pavlovian generalization of fear-potentiated startle and maladaptive generalized avoidance. Further, moderating effects of DS were most pronounced for more ambiguous cues of threat (i.e., stimuli moderately resembling CS+), while moderating effects of DE were most pronounced for more certain cues of threat (i.e., stimuli highly resembling CS+, as well as the CS + itself). Results implicate DS and DE as protective factors against the maladaptive behavioral consequences of Pavlovian generalization, and further indicate that the protective influence of these traits may depend on the ambiguity of the threat at hand.

Gradients of fear: How perception influences fear generalization

The current experiment investigated whether overgeneralization of fear could be due to an inability to perceptually discriminate the initial fear-evoking stimulus from similar stimuli, as fear learning-induced perceptual impairments have been reported but their influence on generalization gradients remain to be elucidated. Three hundred and sixty-eight healthy volunteers participated in a differential fear conditioning paradigm with circles of different sizes as conditioned stimuli (CS), of which one was paired to an aversive IAPS picture. During generalization, each subject was presented with one of 10 different sized circles including the CSs, and were asked to categorize the stimulus as either a CS or as novel after fear responses were recorded. Linear mixed models were used to investigate differences in fear generalization gradients depending on the participant's perception of the test stimulus. We found that the incorrect perception of a novel stimulus as the initial fear-evoking stimulus strongly boosted fear responses. The current findings demonstrate that a significant number of novel stimuli used to assess generalization are incorrectly identified as the initial fear-evoking stimulus, providing a perceptual account for the observed overgeneralization in panic and anxiety disorders. Accordingly, enhancing perceptual processing may be a promising treatment for targeting excessive fear generalization.

A novel perceptual discrimination training task: Reducing fear overgeneralization in the context of fear learning

Generalization is an adaptive learning mechanism, but it can be maladaptive when it occurs in excess. A novel perceptual discrimination training task was therefore designed to moderate fear overgeneralization. We hypothesized that improvement in basic perceptual discrimination would translate into lower fear overgeneralization in affective cues. Seventy adults completed a fear-conditioning task prior to being allocated into training or placebo groups. Predesignated geometric shape pairs were constructed for the training task. A target shape from each pair was presented. Thereafter, participants in the training group were shown both shapes and asked to identify the image that differed from the target. Placebo task participants only indicated the location of each shape on the screen. All participants then viewed new geometric pairs and indicated whether they were identical or different. Finally, participants completed a fear generalization test consisting of perceptual morphs ranging from the CS + to the CS-. Fear-conditioning was observed through physiological and behavioural measures. Furthermore, the training group performed better than the placebo group on the assessment task and exhibited decreased fear generalization in response to threat/safety cues. The findings offer evidence for the effectiveness of the novel discrimination training task, setting the stage for future research with clinical populations.