Overgeneralization Of Fear Research Articles

Comparison of Resting-State Functional Connectivity Between Generalized Anxiety Disorder and Social Anxiety Disorder: Differences in the Nucleus Accumbens and Thalamus Network.

Background: Generalized anxiety disorder (GAD) and social anxiety disorder (SAD) are distinguished by whether anxiety is limited to social situations. However, reports on the differences in brain functional networks between GAD and SAD are few. Our objective is to understand the pathogenesis of GAD and SAD by examining the differences in resting brain function between patients with GAD and SAD and healthy controls (HCs). Methods: This study included 21 patients with SAD, 17 patients with GAD, and 30 HCs. Participants underwent psychological assessments and resting-state functional magnetic resonance imaging. Whole-brain analyses were performed to compare resting-state functional connectivity (rsFC) among the groups. In addition, logistic regression analysis was conducted on the rsFC to identify significant differences between GAD and SAD. Results: Patients with SAD and GAD had significantly higher rsFC between the bilateral postcentral gyri and bilateral amygdalae/thalami than HCs. Compared with patients with SAD, those with GAD had significantly higher rsFC between the right nucleus accumbens and bilateral thalami and between the left nucleus accumbens and right thalamus. rsFC between the left nucleus accumbens and right thalamus positively correlated with state anxiety in patients with SAD and GAD, respectively. In addition, logistic regression analysis revealed that the right nucleus accumbens and the right thalamus connectivity could distinguish SAD from GAD. Conclusions: GAD and SAD were distinguished by the right nucleus accumbens and the right thalamus connectivity. Our findings offer insights into the disease-specific neural basis of SAD and GAD. Clinical Trial Registration Number: UMIN000024087. Impact Statement This study is the first to identify a resting state functional connectivity that distinguishes social anxiety disorder (SAD) from generalized anxiety disorder (GAD) and to clarify a common connectivity in both disorders. We found that the connectivity between the right nucleus accumbens and the right thalamus differentiated SAD from GAD. Furthermore, these rsFC differences suggest an underlying basis for fear overgeneralization. Our findings shed light on the pathophysiology of these conditions and could be used as a basis for further studies to improve outcomes for such patients.

The Impact of Continuous and Partial Reinforcement on the Acquisition and Generalization of Human-Conditioned Fear.

Fear over-generalization as a core symptom of anxiety disorders is manifested by fear responses even to safe stimuli that are very dissimilar to the original dangerous stimulus. The present study investigated the effects of two separate conditioned stimuli-unconditioned stimuli (CS-US) pairing procedures on fear acquisition and generalization using a perceptual discrimination fear-conditioning paradigm, with US expectancy ratings and skin conductance response (SCR) as indicators. One group accepted continuous followed by partial CS-US pairings (C-P group); the other group accepted partial followed by continuous CS-US pairings (P-C group). It was found that compared to the P-C group, the C-P group showed stronger perceptual discrimination of CS+ and CS- in the fear acquisition and showed weaker SCRs and stronger extinction of US expectancy in the generalization. These findings emphasize that CS-US pairings significantly influence fear acquisition and generalization and suggest that continuous-following partial CS-US pairings promote individual discrimination of threat and safety signals and inhibit the generalization of conditioned fear. The results of this study have implications for clinical interventions for patients experiencing negative events.

Anhedonia is associated with overgeneralization of conditioned fear during late adolescence and early adulthood

BackgroundPavlovian fear paradigms involve learning to associate cues with threat or safety. Aberrances in Pavlovian fear learning correlate with psychopathology, especially anxiety disorders. This study evaluated symptom dimensions of anxiety and depression in relation to Pavlovian fear acquisition and generalization. Methods256 participants (70.31 % female) completed a Pavlovian fear acquisition and generalization paradigm at ages 18–19 and 21–22 years. Analyses focused on indices of learning (self-reported US expectancy, skin conductance). Multilevel models tested associations with orthogonal symptom dimensions (Anhedonia-Apprehension, Fears, General Distress) at each timepoint. ResultsAll dimensions were associated with weaker acquisition of US expectancies at each timepoint. Fears was associated with overgeneralization only at age 21–22. General Distress was associated with overgeneralization only at age 18–19. Anhedonia-Apprehension was associated with overgeneralization at ages 18–19 and 21–22. ConclusionsAnhedonia-Apprehension disrupts Pavlovian fear acquisition and increases overgeneralization of fear. These effects may emerge during adolescence and remain into young adulthood. General Distress and Fears also contribute to overgeneralization of fear, but these effects may vary as prefrontal mechanisms of fear inhibition continue to develop during late adolescence. Targeting specific symptom dimensions, particularly Anhedonia-Apprehension, may decrease fear generalization and augment interventions built on Pavlovian principles, such as exposure therapy.

GABAergic interneurons in the hippocampal CA1 mediate contextual fear generalization in PTSD rats.

Fear overgeneralization is widely accepted as a pathogenic marker of post-traumatic stress disorder (PTSD). Recently, GABAergic interneurons have been regarded as key players in the regulation of fear memory. The role of hippocampal GABAergic interneurons in contextual fear generalization of PTSD remains incompletely understood. In the present study, we established a rat model of PTSD with inescapable foot shocks (IFS) and observed the loss of GABAergic interneuron phenotype in the hippocampal cornu ammonis-1 (CA1) subfield. To determine whether the loss of GABAergic interneuron phenotype was associated with fear generalization in PTSD rats, we used adeno-associated virus (AAV) to reduce the expression of GAD67 in CA1 and observed its effect on fear generalization. The results showed that the reduction of GAD67 in CA1 enhanced contextual fear generalization in rats. We investigated whether the PERK pathway was involved in the GABAergic interneuron injury. Increased expression of p-PERK, CHOP, and Caspase12 in GABAergic interneurons of PTSD rats was observed. Then, we used salubrinal, an endoplasmic reticulum stress inhibitor, to modulate the PERK pathway. The salubrinal treatment significantly protected the GABAergic interneurons and relieved fear generalization in PTSD rats. In addition, the results showed that salubrinal down-regulated the expression of CHOP and Caspase12 in GABAergic interneurons of PTSD rats. In conclusion, this study provided evidence that the loss of GABAergic interneuron phenotype in CA1 may contribute to contextual fear generalization in PTSD. The PERK pathway is involved in the GABAergic interneuron injury of PTSD rats and modulating it can protect GABAergic interneurons and constrain contextual fear generalization.

Maladaptation of dentate gyrus mossy cells mediates contextual discrimination deficit after traumatic stress

Fear overgeneralization is a maladaptive response to traumatic stress that is associated with the inability to discriminate between threat and safety contexts, a hallmark feature of post-traumatic stress disorder (PTSD). However, the neural mechanisms underlying this deficit remain unclear. Here, we show that traumatic stress exposure impairs contextual discrimination between threat and safety contexts in the learned helplessness (LH) model. Mossy cells (MCs) in the dorsal hippocampus are suppressed in response to traumatic stress. Bidirectional manipulation of MC activity in the LH model reveals that MC inhibition is causally linked to impaired contextual discrimination. Mechanistically, MC inhibition increases the number of active granule cells in a given context, significantly overlapping context-specific ensembles. Our study demonstrates that maladaptive inhibition of MCs after traumatic stress is a substantial mechanism underlying fear overgeneralization with contextual discrimination deficit, suggesting a potential therapeutic target for cognitive symptoms of PTSD.

Chemogenetic inhibition of central amygdala CRF-expressing neurons decreases alcohol intake but not trauma-related behaviors in a rat model of post-traumatic stress and alcohol use disorder

Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are often comorbid. Few treatments exist to reduce comorbid PTSD/AUD. Elucidating the mechanisms underlying their comorbidity could reveal new avenues for therapy. Here, we employed a model of comorbid PTSD/AUD, in which rats were subjected to a stressful shock in a familiar context followed by alcohol drinking. We then examined fear overgeneralization and irritability in these rats. Familiar context stress elevated drinking, increased fear overgeneralization, increased alcohol-related aggressive signs, and elevated peripheral stress hormones. We then examined transcripts of stress- and fear-relevant genes in the central amygdala (CeA), a locus that regulates stress-mediated alcohol drinking. Compared with unstressed rats, stressed rats exhibited increases in CeA transcripts for Crh and Fkbp5 and decreases in transcripts for Bdnf and Il18. Levels of Nr3c1 mRNA, which encodes the glucocorticoid receptor, increased in stressed males but decreased in stressed females. Transcripts of Il18 binding protein (Il18bp), Glp-1r, and genes associated with calcitonin gene-related peptide signaling (Calca, Ramp1, Crlr-1, and Iapp) were unaltered. Crh, but not Crhr1, mRNA was increased by stress; thus, we tested whether inhibiting CeA neurons that express corticotropin-releasing factor (CRF) suppress PTSD/AUD-like behaviors. We used Crh-Cre rats that had received a Cre-dependent vector encoding hM4D(Gi), an inhibitory Designer Receptors Exclusively Activated by Designer Drugs. Chemogenetic inhibition of CeA CRF neurons reduced alcohol intake but not fear overgeneralization or irritability-like behaviors. Our findings suggest that CeA CRF modulates PTSD/AUD comorbidity, and inhibiting CRF neural activity is primarily associated with reducing alcohol drinking but not trauma-related behaviors that are associated with PTSD/AUD.

Generalized fear after acute stress is caused by change in neuronal cotransmitter identity.

Overgeneralization of fear to harmless situations is a core feature of anxiety disorders resulting from acute stress, yet the mechanisms by which fear becomes generalized are poorly understood. In this study, we show that generalized fear in mice results from a transmitter switch from glutamate to γ-aminobutyric acid (GABA) in serotonergic neurons of the lateral wings of the dorsal raphe. Similar change in transmitter identity was found in the postmortem brains of individuals with posttraumatic stress disorder (PTSD). Overriding the transmitter switch in mice prevented the acquisition of generalized fear. Corticosterone release and activation of glucocorticoid receptors mediated the switch, and prompt antidepressant treatment blocked the cotransmitter switch and generalized fear. Our results provide important insight into the mechanisms involved in fear generalization.

Overgeneralization of conditioned fear in patients with social anxiety disorder.

While abnormal responses to threat, including overgeneralization to conditioned fear, have been postulated to play a critical role in pathological anxiety, the relevance of previous findings to social anxiety disorder (SAD) is unclear. We investigated conditioned and generalized fear responses in patients with SAD using socially relevant stimuli. A total of 26 patients with SAD and 25 healthy controls participated in a fear conditioning and generalization paradigm consisting of two neutral faces as conditioned stimuli (CS+ or CS-) and an angry face with contemptuous comments as unconditioned stimuli. Eight morphed faces of two conditioned stimuli in each continuum were given to test generalization. Behavioral data and physiological responses were acquired. Successful conditioning was observed in the risk ratings for both groups, while only a marginal indication of conditioning was noted in physiological measures. During the generalization phase, patients rated the risk higher than CS- when the stimuli close to CS- contained a portion of CS+ features. Larger skin conductance responses to this stimulus were linked to higher fear of negative evaluation. In addition, patients spent a longer time evaluating safe and ambiguous stimuli than healthy controls and exhibited consistently high levels of subjective arousal. Taken together, our findings suggest that SAD patients may exhibit a tendency towards overgeneralization of fear responses and show distinct patterns in processing generalized threat stimuli compared to healthy controls. Even though overgeneralization was not evident in physiological measures, it is necessary to consider this behavioral characteristic in the clinical management of patients with SAD.

Fear conditioning and fear generalization in children and adolescents with anxiety disorders

Overgeneralization of conditioned fear is associated with anxiety disorders (AD). Most results stem from studies done in adult patients, but studies with children are rare, although the median onset of anxiety disorders lies already in childhood. Thus, the goal of the present study was to examine fear learning and generalization in youth participants, aged 10–17 years, with AD (n = 39) compared to healthy controls (HC) (n = 40). A discriminative fear conditioning and generalization paradigm was used. Ratings of arousal, valence, and US expectancy (the probability of an aversive noise following each stimulus) were measured, hypothesizing that children with AD compared to HC would show heightened ratings of arousal and US expectancy, and decreased positive valence ratings, respectively, as well as overgeneralization of fear. The results indicated that children with AD rated all stimuli as more arousing and less pleasant, and demonstrated higher US expectancy ratings to all stimuli when compared to HC. Thus, rather than displaying qualitatively different generalization patterns (e.g., a linear vs. quadratic slope of the gradient), differences between groups were more quantitative (similar, but parallel shifted gradient). Therefore, overgeneralization of conditioned fear does not seem to be a general marker of anxiety disorders in children and adolescents.

No influence of threat uncertainty on fear generalization.

Fear overgeneralization and perceived uncertainty about future outcomes have been suggested as risk factors for clinical anxiety. However, little is known regarding how they influence each other. In this study, we investigated whether different levels of threat uncertainty influence fear generalization. Three groups of healthy participants underwent a differential fear conditioning protocol followed by a generalization test. All groups learned to associate one female face (conditioned stimulus, CS+) with a female scream (unconditioned stimulus, US), whereas the other face (CS-) was not associated with the scream. In order to manipulate threat uncertainty, one group (low uncertainty, n = 26) received 80%, the second group (moderate uncertainty, n = 32) received 60%, and the third group (high uncertainty, n = 30) 40% CS-US contingency. In the generalization test, all groups saw CS+ and CS- again along with four morphs resembling the CSs in steps of 20%. Subjective (expectancy, valence, and arousal ratings), psychophysiological (skin conductance response, SCR), and visuocortical (steady-state visual evoked potentials, ssVEPs) indices of fear were registered. Participants expected the US according to their reinforcement schedules and the discriminative responses to CS+/CS- increased with more uncertainty in skin conductance. However, acquisition of conditioned fear was not evident in ssVEPs. During the generalization test, we found no effect of threat uncertainty in any of the measured variables, but the strength of generalization for threat expectancy ratings was positively correlated with dispositional intolerance of uncertainty. This study suggests that mere threat uncertainty does not modulate fear generalization.

The overgeneralization of pain-related fear in individuals with higher pain sensitivity: A behavioral and event-related potential study

Fear generalization contributes to the development and maintenance of pain. Pain sensitivity has been proposed to predict the strength of fear responses to aversive stimuli. However, whether individual variation in pain sensitivity affects pain-related fear generalization and its underlying cognitive processing remains unclear. To address this gap, we recorded behavioral and event-related potential (ERP) data among 22 high pain sensitivity (HPS) and 22 low pain sensitivity (LPS) healthy adults when exposed to a fear generalization paradigm. The behavioral results indicate that the HPS group displayed higher unconditioned stimulus expectancy and greater fear, arousal, and anxiety ratings to conditioned stimulus and generalization stimulus than the LPS group (all p values < 0.05). The ERP results showed that the HPS group exhibited a larger late positive potential evoked by GS2, GS3 and CS- (all p < 0.005) but a smaller N1 evoked by all CS and GSs (all p values < 0.05) relative to the LPS group. These findings suggest that individuals with a high level of pain sensitivity allocate more attention resources to pain-related threatening stimuli, which contributes to an overgeneralization of pain-related fear.

The excessive generalization of fear affected by perceptual bias in experimental pain individuals: Evidence from an event-related potential study.

Excessiv generalization of fear contributes to the development and maintenance of pain. Prior research has demonstrated the importance of perception in fear generalization and found that individuals in painful conditions exhibited perceptual bias. However, the extent to which perceptual bias in pain affects the generalization of pain-related fear and its underlying neural activity remains unclear. Here, we tested whether perceptual bias in experimental pain individuals led to the overgeneralization of pain-related fear by recording behavioral and neural responses. To this end, we established an experimental pain model by spraying capsaicin on the surface of the seventh cervical vertebra of the participant. A total of 23 experimental pain participants and 23 matched nonpain controls learned fear conditioning and then completed the fear generalization paradigm combined with the perceptual categorization task. We found that the novel and safety cues were more likely to be identified as threat cues in the experimental group, resulting in higher US expectancy ratings compared to the control group. The event-related potential results showed that the experimental group exhibited earlier N1 latency and smaller P1 and late positive potential amplitudes than those in the control group. Our findings suggest that the experimental pain individuals exhibited an excessive generalization of fear affected by perceptual bias and reduced their attentional allocation to pain-related fear stimuli.

Chronic unilateral inhibition of GABA synthesis in the amygdala increases specificity of conditioned fear in a discriminative fear conditioning paradigm in rats

Neural activity in the amygdala is critical for fear learning. In anxiety disorder patients, bilateral hyperactivity of the amygdala can be observed. This hyperactivation is often associated with the facilitation of fear learning and/or over-generalization of conditioned fear. In contrast, hypoactivity of the amygdala, e.g. by pharmacological interventions, attenuates or blocks fear learning. To date, little is known about how neural excitability of the amygdala affects specificity or generalization of fear. Therefore, the present study utilized chronic inhibition of GABA synthesis in the amygdala to increase excitability and investigated the effect on the specificity of fear learning. In rats, unilateral cannulas aiming at the amygdala were implanted. The cannulas were connected to subcutaneously implanted osmotic mini pumps that delivered either the GABA synthesis inhibitor L-allylglycine or its inactive enantiomer D-allylglycine. Following one week of chronic GABA synthesis manipulation, the rats were submitted to a discriminative fear conditioning protocol. In addition, anxiety-like behavior in the light-dark box was measured. Our data show that chronic unilateral L-AG infusions into the amygdala improve the specificity of learned fear, support safety learning, and reduce fear generalization and anxiety. This data demonstrates that moderately increased amygdala excitability can be beneficial for the specificity of fear learning and highlights the potential application for therapeutic interventions.

Age-related deficits in neuronal physiology and cognitive function are recapitulated in young mice overexpressing the L-type calcium channel, CaV 1.3.

The calcium dysregulation hypothesis of brain aging posits that an age-related increase in neuronal calcium concentration is responsible for alterations in a variety of cellular processes that ultimately result in learning and memory deficits in aged individuals. We previously generated a novel transgenic mouse line, in which expression of the L-type voltage-gated calcium, CaV 1.3, is increased by ~50% over wild-type littermates. Here, we show that, in young mice, this increase is sufficient to drive changes in neuronal physiology and cognitive function similar to those observed in aged animals. Specifically, there is an increase in the magnitude of the postburst afterhyperpolarization, a deficit in spatial learning and memory (assessed by the Morris water maze), a deficit in recognition memory (assessed in novel object recognition), and an overgeneralization of fear to novel contexts (assessed by contextual fear conditioning). While overexpression of CaV 1.3 recapitulated these key aspects of brain aging, it did not produce alterations in action potential firing rates, basal synaptic communication, or spine number/density. Taken together, these results suggest that increased expression of CaV 1.3 in the aged brain is a crucial factor that acts in concert with age-related changes in other processes to produce the full complement of structural, functional, and behavioral outcomes that are characteristic of aged animals.

Effects of intra-hippocampal corticosterone and sleep on consolidation of memories of aversive experience in rats

Formation and consolidation of memories for highly stressful (traumatic) events is a complex process that involves interplay between multiple memory systems and has implications for etiology and treatment of stress- and trauma-related disorders. Here we study effects of sleep/wake states and high intra-hippocampal corticosterone on consolidation of aversive contextual memories, as well as consolidation of association between auditory unpaired phasic background cues and fear response in rats. Animals were implanted with EEG and EMG electrodes for sleep assessment and cannulas for intra-hippocampal corticosterone application. They were familiarized to a “safe box” and then trained in a fear conditioning paradigm in a distinct “shock box” with a prominent unpaired phasic background auditory cue. Immediately after conditioning, animals received bilateral intra-hippocampal saline (1 μl) or corticosterone (10 ng in 1 μl) injection and were either allowed to sleep or were kept awake for a following two-hour consolidation period. Memory tests 24 h later revealed that the saline-injected animals that slept during consolidation had significantly stronger fear responses in the shock box compared to the safe box as well as increased fear response in response to the auditory cue. Lack of sleep during the consolidation period in saline injected animals led to generalization of the fear response to the safe context, while association between auditory cue and fear response was preserved. High intra-hippocampal corticosterone levels during memory consolidation led to generalization of fear response to the safe context, regardless of sleep/wake state, while enhancement of response to auditory cue was not observed. Our results show how manipulation of conditions during consolidation can lead to greatly variable memories for an aversive episode with distinct behavioral outcomes. Observed overgeneralization of fear to safe context and altered fear response to background phasic cue has implications for understanding etiology of pathological memory alternations in stress-related conditions e.g., in posttraumatic stress disorder in humans.

FKBP5 inhibitors modulate alcohol drinking and trauma-related behaviors in a model of comorbid post-traumatic stress and alcohol use disorder.

Post-traumatic stress disorder (PTSD) leads to enhanced alcohol drinking and development of alcohol use disorder (AUD). Identifying shared neural mechanisms might help discover new therapies for PTSD/AUD. Here, we employed a rat model of comorbid PTSD/AUD to evaluate compounds that inhibit FK506-binding protein 51 (FKBP5), a co-chaperone modulator of glucocorticoid receptors implicated in stress-related disorders. Male and female rats received a familiar avoidance-based shock stress followed by voluntary alcohol drinking. We then assessed trauma-related behaviors through sleep bout cycles, hyperarousal, fear overgeneralization, and irritability. To evaluate the role of stress and alcohol history on the sensitivity to FKBP5 inhibitors, in two separate studies, we administered two FKBP5 inhibitors, benztropine (Study 1) or SAFit2 (Study 2). FKBP5 inhibitors were administered on the last alcohol drinking session and prior to each trauma-related behavioral assessment. We also measured plasma corticosterone to assess the actions of FKBP5 inhibitors after familiar shock stress and alcohol drinking. Benztropine reduced alcohol preference in stressed males and females, while aggressive bouts were reduced in benztropine-treated stressed females. During hyperarousal, benztropine reduced several startle responseoutcomes across stressed males and females. Corticosterone was reduced in benztropine-treated stressed males. The selective FKBP5 inhibitor, SAFit2, reduced alcohol drinking in stressed males but not females, with no differences in irritability. Importantly, SAFit2 decreased fear overgeneralization in stressed males and females. SAFit2 also reduced corticosterone across stressed males and females. Neither FKBP5 inhibitor changed sleep bout structure. These findings indicate that FKBP5 inhibitors modulate stress-related alcohol drinking and partially modulate trauma-related behaviors. This work supports the hypothesis that targeting FKBP5 may alleviate PTSD/AUD comorbidity.

Childhood Maltreatment in Females Is Associated with Enhanced Fear Acquisition and an Overgeneralization of Fear.

Childhood maltreatment may alter fear neurocircuitry, which results in pathological anxiety and depression. One alteration of fear-related behaviors that has been observed in several psychiatric populations is an overgeneralization of fear. Thus, we examined the association between childhood maltreatment and fear generalization in a non-clinical sample of young adults. Two hundred and ninety-one participants underwent differential fear conditioning in a fear-potentiated startle paradigm. One visual stimulus (CS+), but not another (CS-), was associated with an aversive airblast to the throat (US) during acquisition. The next day, participants were tested for their fear responses to the CS+, CS-, and several generalization stimuli (GS) without the presence of the US. Participants also completed questionnaires that assessed symptoms of childhood maltreatment, anxiety, depression, and post-traumatic stress disorder (PTSD). Participants reporting high childhood maltreatment (n = 71; 23 males, 48 females) exhibited significantly greater anxiety, depression, and symptoms of PTSD than participants reporting low childhood maltreatment (n = 220; 133 males, 87 females). Females reporting high childhood maltreatment demonstrated significantly enhanced fear learning and greater fear generalization, based on their fear-potentiated startle responses. Our findings suggest that childhood maltreatment may sex-dependently influence the development of fear neurocircuitry and result in greater fear generalization in maltreated females.

Stimulus diversity increases category-based fear generalization and the effect of intolerance of uncertainty

Fear generalization refers to conditioned fear responses extending to related stimuli and fear overgeneralization is a key feature of pathological anxiety. Along with perception similarity, conceptual relations affect fear generalization. We investigated whether stimulus diversity–an important principle of category-based induction–influences fear generalization. Induction studies have shown that generalization from a premise involving diverse instances is stronger than that from non-diverse instances. We adopted this framework for fear learning and established two groups. The diverse group developed fear in response to diverse instances from one category, while the non-diverse group acquired fear of non-diverse instances from the same category. An effect of stimulus diversity was observed in shock-expectancy ratings, with the diverse group displaying higher fear generalization than the non-diverse group. We also tested whether intolerance of uncertainty (IU) might affect the difference in fear generalization between the two conditions. Individuals with higher IU showed reduced difference in fear generalization between two conditions, mainly driven by heightened fear generalization to novel stimulus with ambiguous threat levels in the non-diverse condition. This study helps illustrate the mechanisms behind differential category-based fear generalization and provides a potential explanation for why higher IU individuals may develop anxiety disorders following trauma.

Generalization of threats attributed to large carnivores in areas of high human-wildlife conflict.

Fear-induced generalization of threats to noninimical stimuli is a behavioral tendency of humans to minimize exposure to potential threats. In human-carnivore conflict zones, people often generalize their fear of predation by obligate carnivores to nonobligate carnivores despite differences in species' predation rates. We investigated the effect of a perceived threat of large obligate carnivores to livestock on tolerance and perception of striped hyena (Hyaena hyaena) in an area of high human-carnivore conflict. We surveyed 197 households through asemistructured questionnaire to determine people's perception and tolerance of striped hyenas in Sathyamangalam and Mudumalai Tiger Reserves after identification of the current distribution range of hyena determined through camera trap and sign surveys. Through the random forest algorithm, we modeled the level of tolerance of striped hyena as a function of loss of livestock to predation and from disease, the perceived threat of predation by hyena, and other socioeconomic attributes. Animal husbandry was a major source of income but was severely affected by livestock loss due to predation and disease. Sixty-nine percent of people were uncertain about predatory behavior of hyena; out of that, 23% reported a negative conservation attitude. Only 6 instances of hyena depredation on livestock and 2 on dogs were reported. Our model confirmed that economic instability associated with increased loss to predation and disease, livestock dependency, and a decrease in family annual income negatively affected people's tolerance of hyena. Perceptual uncertainty related to predatory behavior of hyena also negatively affected people's tolerance. In our study area, economic instability and perceptual uncertainty led to generalization of fear of large carnivores to a nonobligate predator. Such generalization may affect the attitude of people toward many other species. Understanding the role of economic instability and perceptual uncertainty should facilitate conservation of species, such as the hyena, that are vulnerable to false generalization.

The effect of partial and continuous reinforcement on the generalization of conditioned fear in humans

The popular paradigm of Pavlovian conditioned fear has been used to study learning and memory processes that mediate anxiety disorder. Fear extinction studies have often paired the conditioned stimulus (CS) and the unconditioned stimulus (US) on a subset of acquisition trials (partial reinforcement) to prolong extinction. However, there have been few studies on the effect of partial reinforcement and continuous reinforcement on fear generalization. To better understand the influence of the CS–US pairing rate on fear generalization, the experimenters used CSs paired with US at 50% (CS50), 75% (CS75), and 100% (CS100) during fear conditioning. A total of 66 participants, who were assigned at random to the different reinforcement rates, underwent fear acquisition and generalization tests on expectancy ratings and skin conductance responses. The continuous reinforcement group (CS100) showed a flatter generalization gradient, while the partial reinforcement groups (CS50, CS75) showed increased generalization magnitudes. These results suggest that the partial reinforcement extinction effect is related to threat intensity, whereas continuous reinforcement produces threat-sensitivity fear generalization, which has been used to explain the overgeneralization of fear.