11 recherche sur le mot-clé 'fear conditioning'

Age-Dependent Effects of Loss of Contactin-Associated Protein-Like 2, an Autism-Associated Gene, on the Acquisition and Recall of Fear Memory / A. BERNS ; Myles JONES ; A. TOWNSEND ; A.K. EAGEN ; Sarah L. FERRI ; D.R. LANGBEHN ; H. JANOUSCHEK in Autism Research, 18-5 (May 2025)  

Public ISBD [article]  inAutism Research > 18-5 (May 2025) . - p.1011-1023 Titre : Age-Dependent Effects of Loss of Contactin-Associated Protein-Like 2, an Autism-Associated Gene, on the Acquisition and Recall of Fear Memory Type de document : texte imprimé Auteurs : A. BERNS, Auteur ; Myles JONES, Auteur ; A. TOWNSEND, Auteur ; A.K. EAGEN, Auteur ; Sarah L. FERRI, Auteur ; D.R. LANGBEHN, Auteur ; H. JANOUSCHEK, Auteur Article en page(s) : p.1011-1023 Langues : Anglais (eng) Mots-clés : anxiety  autism spectrum disorder  CASPR2  Cntnap2  development  fear  fear conditioning  memory Index. décimale : PER Périodiques Résumé : ABSTRACT The contactin-associated protein-like 2 (Cntnap2) gene is relevant to autism spectrum disorder (ASD), which is associated with age-specific structural alterations in limbic brain regions. The Cntnap2 gene encodes for the contactin-associated protein-like 2 (CASPR2) protein, and CASPR2 protein levels are high in the amygdala, a limbic region that is essential for the processing of fear and anxiety. In humans, reduced levels of this protein arising from CNTNAP2 mutations could potentially account for the autism-associated increase in fear and anxiety. Here, we report the extent to which loss of CASPR2 in mice contributes to the development of fear- and anxiety-related behaviors. Pavlovian fear conditioning experiments revealed that loss of CASPR2 has age-dependent effects on the acquisition of fear memory, recall of both cue-evoked and context-related fear memory, and stability of cue-evoked fear memory. Additionally, data from the elevated zero maze suggest that CASPR2 deficiency contributes to anxiety-related behaviors, especially in juvenile (29-day old) mice. These are the first reports of age-dependent effects of CASPR2 deficiency on fear and anxiety-related behaviors, and they set the stage for a better understanding of developmental alterations of fear and anxiety in ASD. En ligne : https://doi.org/10.1002/aur.70034 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=558 [article] Age-Dependent Effects of Loss of Contactin-Associated Protein-Like 2, an Autism-Associated Gene, on the Acquisition and Recall of Fear Memory [texte imprimé] / A. BERNS, Auteur ; Myles JONES, Auteur ; A. TOWNSEND, Auteur ; A.K. EAGEN, Auteur ; Sarah L. FERRI, Auteur ; D.R. LANGBEHN, Auteur ; H. JANOUSCHEK, Auteur . - p.1011-1023. Langues : Anglais (eng) in Autism Research > 18-5 (May 2025) . - p.1011-1023 Mots-clés : anxiety  autism spectrum disorder  CASPR2  Cntnap2  development  fear  fear conditioning  memory Index. décimale : PER Périodiques Résumé : ABSTRACT The contactin-associated protein-like 2 (Cntnap2) gene is relevant to autism spectrum disorder (ASD), which is associated with age-specific structural alterations in limbic brain regions. The Cntnap2 gene encodes for the contactin-associated protein-like 2 (CASPR2) protein, and CASPR2 protein levels are high in the amygdala, a limbic region that is essential for the processing of fear and anxiety. In humans, reduced levels of this protein arising from CNTNAP2 mutations could potentially account for the autism-associated increase in fear and anxiety. Here, we report the extent to which loss of CASPR2 in mice contributes to the development of fear- and anxiety-related behaviors. Pavlovian fear conditioning experiments revealed that loss of CASPR2 has age-dependent effects on the acquisition of fear memory, recall of both cue-evoked and context-related fear memory, and stability of cue-evoked fear memory. Additionally, data from the elevated zero maze suggest that CASPR2 deficiency contributes to anxiety-related behaviors, especially in juvenile (29-day old) mice. These are the first reports of age-dependent effects of CASPR2 deficiency on fear and anxiety-related behaviors, and they set the stage for a better understanding of developmental alterations of fear and anxiety in ASD. En ligne : https://doi.org/10.1002/aur.70034 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=558

Better fear conditioning is associated with reduced symptom severity in autism spectrum disorders / Mikle SOUTH in Autism Research, 4-6 (December 2011)  

Public ISBD [article]  inAutism Research > 4-6 (December 2011) . - p.412-421 Titre : Better fear conditioning is associated with reduced symptom severity in autism spectrum disorders Type de document : texte imprimé Auteurs : Mikle SOUTH, Auteur ; Michael J. LARSON, Auteur ; Sarah E. WHITE, Auteur ; Julianne DANA, Auteur ; Michael J. CROWLEY, Auteur Année de publication : 2012 Article en page(s) : p.412-421 Langues : Anglais (eng) Mots-clés : autism spectrum disorders  amygdala  anxiety  fear conditioning  dimensional measures Index. décimale : PER Périodiques Résumé : Evidence from behavioral and neuroimaging studies suggest that atypical amygdala function plays a critical role in the development of autism spectrum disorders (ASD). The handful of psychophysiological studies examining amygdala function in ASD using classical fear conditioning paradigms have yielded discordant results. We recorded skin conductance response (SCR) during a simple discrimination conditioning task in 30 children and adolescents (ages 8–18) diagnosed with high-functioning ASD and 30 age- and IQ-matched, typically developing controls. SCR response in the ASD group was uniquely and positively associated with social anxiety; and negatively correlated with autism symptom severity, in particular with social functioning. Fear conditioning studies have tremendous potential to aid understanding regarding the amygdale's role in the varied symptom profile of ASD. Our data demonstrate that such studies require careful attention to task-specific factors, including task complexity; and also to contributions of dimensional, within-group factors that contribute to ASD heterogeneity. En ligne : http://dx.doi.org/10.1002/aur.221 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151 [article] Better fear conditioning is associated with reduced symptom severity in autism spectrum disorders [texte imprimé] / Mikle SOUTH, Auteur ; Michael J. LARSON, Auteur ; Sarah E. WHITE, Auteur ; Julianne DANA, Auteur ; Michael J. CROWLEY, Auteur . - 2012 . - p.412-421. Langues : Anglais (eng) in Autism Research > 4-6 (December 2011) . - p.412-421 Mots-clés : autism spectrum disorders  amygdala  anxiety  fear conditioning  dimensional measures Index. décimale : PER Périodiques Résumé : Evidence from behavioral and neuroimaging studies suggest that atypical amygdala function plays a critical role in the development of autism spectrum disorders (ASD). The handful of psychophysiological studies examining amygdala function in ASD using classical fear conditioning paradigms have yielded discordant results. We recorded skin conductance response (SCR) during a simple discrimination conditioning task in 30 children and adolescents (ages 8–18) diagnosed with high-functioning ASD and 30 age- and IQ-matched, typically developing controls. SCR response in the ASD group was uniquely and positively associated with social anxiety; and negatively correlated with autism symptom severity, in particular with social functioning. Fear conditioning studies have tremendous potential to aid understanding regarding the amygdale's role in the varied symptom profile of ASD. Our data demonstrate that such studies require careful attention to task-specific factors, including task complexity; and also to contributions of dimensional, within-group factors that contribute to ASD heterogeneity. En ligne : http://dx.doi.org/10.1002/aur.221 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151

Characterization of early markers of disease in the mouse model of mucopolysaccharidosis IIIB / Katherine B. MCCULLOUGH in Journal of Neurodevelopmental Disorders, 16 (2024)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 16 (2024) Titre : Characterization of early markers of disease in the mouse model of mucopolysaccharidosis IIIB Type de document : texte imprimé Auteurs : Katherine B. MCCULLOUGH, Auteur ; Amanda TITUS, Auteur ; Kate REARDON, Auteur ; Sara CONYERS, Auteur ; Joseph D. DOUGHERTY, Auteur ; Xia GE, Auteur ; Joel R. GARBOW, Auteur ; Patricia DICKSON, Auteur ; Carla M. YUEDE, Auteur ; Susan E. MALONEY, Auteur Langues : Anglais (eng) Mots-clés : Humans  Animals  Adult  Child  Mucopolysaccharidosis III/genetics/pathology  Diffusion Tensor Imaging  Brain  Disease Models, Animal  Treatment Outcome  Aggression  Dominance  Fear conditioning  Gait  Lysosomal storage disorder  Mri/dti  Mucopolysaccharidosis IIIB  Sanfilippo B  Startle response  Ultrasonic vocalization Index. décimale : PER Périodiques Résumé : BACKGROUND: Mucopolysaccharidosis (MPS) IIIB, also known as Sanfilippo Syndrome B, is a devastating childhood disease. Unfortunately, there are currently no available treatments for MPS IIIB patients. Yet, animal models of lysosomal storage diseases have been valuable tools in identifying promising avenues of treatment. Enzyme replacement therapy, gene therapy, and bone marrow transplant have all shown efficacy in the MPS IIIB model systems. A ubiquitous finding across rodent models of lysosomal storage diseases is that the best treatment outcomes resulted from intervention prior to symptom onset. Therefore, the aim of the current study was to identify early markers of disease in the MPS IIIB mouse model as well as examine clinically-relevant behavioral domains not yet explored in this model. METHODS: Using the MPS IIIB mouse model, we explored early developmental trajectories of communication and gait, and later social behavior, fear-related startle and conditioning, and visual capabilities. In addition, we examined brain structure and function via magnetic resonance imaging and diffusion tensor imaging. RESULTS: We observed reduced maternal isolation-induced ultrasonic vocalizations in MPS IIIB mice relative to controls, as well as disruption in a number of the spectrotemporal features. MPS IIIB also exhibited disrupted thermoregulation during the first two postnatal weeks without any differences in body weight. The developmental trajectories of gait were largely normal. In early adulthood, we observed intact visual acuity and sociability yet a more submissive phenotype, increased aggressive behavior, and decreased social sniffing relative to controls. MPS IIIB mice showed greater inhibition of startle in response to a pretone with a decrease in overall startle response and reduced cued fear memory. MPS IIIB also weighed significantly more than controls throughout adulthood and showed larger whole brain volumes and normalized regional volumes with intact tissue integrity as measured with magnetic resonance and diffusion tensor imaging, respectively. CONCLUSIONS: Together, these results indicate disease markers are present as early as the first two weeks postnatal in this model. Further, this model recapitulates social, sensory and fear-related clinical features. Our study using a mouse model of MPS IIIB provides essential baseline information that will be useful in future evaluations of potential treatments. En ligne : https://dx.doi.org/10.1186/s11689-024-09534-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575 [article] Characterization of early markers of disease in the mouse model of mucopolysaccharidosis IIIB [texte imprimé] / Katherine B. MCCULLOUGH, Auteur ; Amanda TITUS, Auteur ; Kate REARDON, Auteur ; Sara CONYERS, Auteur ; Joseph D. DOUGHERTY, Auteur ; Xia GE, Auteur ; Joel R. GARBOW, Auteur ; Patricia DICKSON, Auteur ; Carla M. YUEDE, Auteur ; Susan E. MALONEY, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 16 (2024) Mots-clés : Humans  Animals  Adult  Child  Mucopolysaccharidosis III/genetics/pathology  Diffusion Tensor Imaging  Brain  Disease Models, Animal  Treatment Outcome  Aggression  Dominance  Fear conditioning  Gait  Lysosomal storage disorder  Mri/dti  Mucopolysaccharidosis IIIB  Sanfilippo B  Startle response  Ultrasonic vocalization Index. décimale : PER Périodiques Résumé : BACKGROUND: Mucopolysaccharidosis (MPS) IIIB, also known as Sanfilippo Syndrome B, is a devastating childhood disease. Unfortunately, there are currently no available treatments for MPS IIIB patients. Yet, animal models of lysosomal storage diseases have been valuable tools in identifying promising avenues of treatment. Enzyme replacement therapy, gene therapy, and bone marrow transplant have all shown efficacy in the MPS IIIB model systems. A ubiquitous finding across rodent models of lysosomal storage diseases is that the best treatment outcomes resulted from intervention prior to symptom onset. Therefore, the aim of the current study was to identify early markers of disease in the MPS IIIB mouse model as well as examine clinically-relevant behavioral domains not yet explored in this model. METHODS: Using the MPS IIIB mouse model, we explored early developmental trajectories of communication and gait, and later social behavior, fear-related startle and conditioning, and visual capabilities. In addition, we examined brain structure and function via magnetic resonance imaging and diffusion tensor imaging. RESULTS: We observed reduced maternal isolation-induced ultrasonic vocalizations in MPS IIIB mice relative to controls, as well as disruption in a number of the spectrotemporal features. MPS IIIB also exhibited disrupted thermoregulation during the first two postnatal weeks without any differences in body weight. The developmental trajectories of gait were largely normal. In early adulthood, we observed intact visual acuity and sociability yet a more submissive phenotype, increased aggressive behavior, and decreased social sniffing relative to controls. MPS IIIB mice showed greater inhibition of startle in response to a pretone with a decrease in overall startle response and reduced cued fear memory. MPS IIIB also weighed significantly more than controls throughout adulthood and showed larger whole brain volumes and normalized regional volumes with intact tissue integrity as measured with magnetic resonance and diffusion tensor imaging, respectively. CONCLUSIONS: Together, these results indicate disease markers are present as early as the first two weeks postnatal in this model. Further, this model recapitulates social, sensory and fear-related clinical features. Our study using a mouse model of MPS IIIB provides essential baseline information that will be useful in future evaluations of potential treatments. En ligne : https://dx.doi.org/10.1186/s11689-024-09534-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575

Childhood adversity is associated with reduced threat-safety discrimination and increased fear generalization in 12- to 16-year-olds / Aleksandra LECEI ; Maarten JACKERS ; Lise JENNEN ; Koen SCHRUERS ; Bram VERVLIET ; Bart BOETS ; Ruud VAN WINKEL in Journal of Child Psychology and Psychiatry, 66-6 (June 2025)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 66-6 (June 2025) . - p.821-833 Titre : Childhood adversity is associated with reduced threat-safety discrimination and increased fear generalization in 12- to 16-year-olds Type de document : texte imprimé Auteurs : Aleksandra LECEI, Auteur ; Maarten JACKERS, Auteur ; Lise JENNEN, Auteur ; Koen SCHRUERS, Auteur ; Bram VERVLIET, Auteur ; Bart BOETS, Auteur ; Ruud VAN WINKEL, Auteur Article en page(s) : p.821-833 Langues : Anglais (eng) Mots-clés : Childhood adversity  fear conditioning  fear generalization  adolescence Index. décimale : PER Périodiques Résumé : Background Childhood adversity poses a major transdiagnostic risk for a host of psychiatric disorders. Altered threat-related information processing has been put forward as a potential process underlying the association between childhood adversity and psychiatric disorders, with previous research providing support for decreased discrimination between threat and safety cues, in both children and adults exposed to adversity. This altered threat-safety discrimination has been hypothesized to stem from increased generalization of fear, yet to date, this hypothesis has not been tested in youth. Methods Here, we investigate whether childhood adversity is associated with fear generalization during adolescence. 119 adolescents between 12 and 16 years of age (mean 13.95), of whom 63 exposed to childhood adversity, completed a fear generalization paradigm. Fear conditioning was assessed through trial-by-trial US expectancy ratings and post-experimental ratings of fear, valence and arousal. Additionally, we administered a perceptual discrimination task to assess the potential impact of perceptual discrimination abilities upon fear generalization. Results In line with our hypotheses, results showed that childhood adversity is associated with (1) reduced threat-safety differentiation during fear acquisition and (2) increased fear generalization in both boys and girls, albeit to a different extent, as boys showed more generalization towards safety cues while girls showed more generalization towards dangerous cues. Moreover, this overgeneralization of fear could not be attributed to group differences in perceptual discrimination. Conclusions Altered fear learning may be an important process through which adversity increases risk for the development of psychopathology. Longitudinal research is essential to elucidate risk and resilience patterns following childhood adversity. En ligne : https://doi.org/10.1111/jcpp.14092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=556 [article] Childhood adversity is associated with reduced threat-safety discrimination and increased fear generalization in 12- to 16-year-olds [texte imprimé] / Aleksandra LECEI, Auteur ; Maarten JACKERS, Auteur ; Lise JENNEN, Auteur ; Koen SCHRUERS, Auteur ; Bram VERVLIET, Auteur ; Bart BOETS, Auteur ; Ruud VAN WINKEL, Auteur . - p.821-833. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 66-6 (June 2025) . - p.821-833 Mots-clés : Childhood adversity  fear conditioning  fear generalization  adolescence Index. décimale : PER Périodiques Résumé : Background Childhood adversity poses a major transdiagnostic risk for a host of psychiatric disorders. Altered threat-related information processing has been put forward as a potential process underlying the association between childhood adversity and psychiatric disorders, with previous research providing support for decreased discrimination between threat and safety cues, in both children and adults exposed to adversity. This altered threat-safety discrimination has been hypothesized to stem from increased generalization of fear, yet to date, this hypothesis has not been tested in youth. Methods Here, we investigate whether childhood adversity is associated with fear generalization during adolescence. 119 adolescents between 12 and 16 years of age (mean 13.95), of whom 63 exposed to childhood adversity, completed a fear generalization paradigm. Fear conditioning was assessed through trial-by-trial US expectancy ratings and post-experimental ratings of fear, valence and arousal. Additionally, we administered a perceptual discrimination task to assess the potential impact of perceptual discrimination abilities upon fear generalization. Results In line with our hypotheses, results showed that childhood adversity is associated with (1) reduced threat-safety differentiation during fear acquisition and (2) increased fear generalization in both boys and girls, albeit to a different extent, as boys showed more generalization towards safety cues while girls showed more generalization towards dangerous cues. Moreover, this overgeneralization of fear could not be attributed to group differences in perceptual discrimination. Conclusions Altered fear learning may be an important process through which adversity increases risk for the development of psychopathology. Longitudinal research is essential to elucidate risk and resilience patterns following childhood adversity. En ligne : https://doi.org/10.1111/jcpp.14092 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=556

CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes / Catherine FRICANO-KUGLER in Molecular Autism, 10 (2019)  

Public ISBD [article]  inMolecular Autism > 10 (2019) . - 25p. Titre : CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes Type de document : texte imprimé Auteurs : Catherine FRICANO-KUGLER, Auteur ; Aaron GORDON, Auteur ; Grace SHIN, Auteur ; Kun GAO, Auteur ; Jenny NGUYEN, Auteur ; Jamee BERG, Auteur ; Mary STARKS, Auteur ; Daniel H. GESCHWIND, Auteur Article en page(s) : 25p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder (ASD)  Cyfip1  Dup15q  Fear conditioning  Mouse behavior  Neurodevelopmental disorders  RNA sequencing Index. décimale : PER Périodiques Résumé : Background: CYFIP1, a protein that interacts with FMRP and regulates protein synthesis and actin dynamics, is overexpressed in Dup15q syndrome as well as autism spectrum disorder (ASD). While CYFIP1 heterozygosity has been rigorously studied due to its loss in 15q11.2 deletion, Prader-Willi and Angelman syndrome, the effects of CYFIP1 overexpression, as is observed in patients with CYFIP1 duplication, are less well understood. Methods: We developed and validated a mouse model of human CYFIP1 overexpression (CYFIP1 OE) using qPCR and western blot analysis. We performed a large battery of behavior testing on these mice, including ultrasonic vocalizations, three-chamber social assay, home-cage behavior, Y-maze, elevated plus maze, open field test, Morris water maze, fear conditioning, prepulse inhibition, and the hot plate assay. We also performed RNA sequencing and analysis on the basolateral amygdala. Results: Extensive behavioral testing in CYFIP1 OE mice reveals no changes in the core behaviors related to ASD: social interactions and repetitive behaviors. However, we did observe mild learning deficits and an exaggerated fear response. Using RNA sequencing of the basolateral amygdala, a region associated with fear response, we observed changes in pathways related to cytoskeletal regulation, oligodendrocytes, and myelination. We also identified GABA-A subunit composition changes in basolateral amygdala neurons, which are essential components of the neural fear conditioning circuit. Conclusion: Overall, this research identifies the behavioral and molecular consequences of CYFIP1 overexpression and how they contribute to the variable phenotype seen in Dup15q syndrome and in ASD patients with excess CYFIP1. En ligne : http://dx.doi.org/10.1186/s13229-019-0278-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402 [article] CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes [texte imprimé] / Catherine FRICANO-KUGLER, Auteur ; Aaron GORDON, Auteur ; Grace SHIN, Auteur ; Kun GAO, Auteur ; Jenny NGUYEN, Auteur ; Jamee BERG, Auteur ; Mary STARKS, Auteur ; Daniel H. GESCHWIND, Auteur . - 25p. Langues : Anglais (eng) in Molecular Autism > 10 (2019) . - 25p. Mots-clés : Autism spectrum disorder (ASD)  Cyfip1  Dup15q  Fear conditioning  Mouse behavior  Neurodevelopmental disorders  RNA sequencing Index. décimale : PER Périodiques Résumé : Background: CYFIP1, a protein that interacts with FMRP and regulates protein synthesis and actin dynamics, is overexpressed in Dup15q syndrome as well as autism spectrum disorder (ASD). While CYFIP1 heterozygosity has been rigorously studied due to its loss in 15q11.2 deletion, Prader-Willi and Angelman syndrome, the effects of CYFIP1 overexpression, as is observed in patients with CYFIP1 duplication, are less well understood. Methods: We developed and validated a mouse model of human CYFIP1 overexpression (CYFIP1 OE) using qPCR and western blot analysis. We performed a large battery of behavior testing on these mice, including ultrasonic vocalizations, three-chamber social assay, home-cage behavior, Y-maze, elevated plus maze, open field test, Morris water maze, fear conditioning, prepulse inhibition, and the hot plate assay. We also performed RNA sequencing and analysis on the basolateral amygdala. Results: Extensive behavioral testing in CYFIP1 OE mice reveals no changes in the core behaviors related to ASD: social interactions and repetitive behaviors. However, we did observe mild learning deficits and an exaggerated fear response. Using RNA sequencing of the basolateral amygdala, a region associated with fear response, we observed changes in pathways related to cytoskeletal regulation, oligodendrocytes, and myelination. We also identified GABA-A subunit composition changes in basolateral amygdala neurons, which are essential components of the neural fear conditioning circuit. Conclusion: Overall, this research identifies the behavioral and molecular consequences of CYFIP1 overexpression and how they contribute to the variable phenotype seen in Dup15q syndrome and in ASD patients with excess CYFIP1. En ligne : http://dx.doi.org/10.1186/s13229-019-0278-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402

Fear Potentiated Startle in Children With Autism Spectrum Disorder: Association With Anxiety Symptoms and Amygdala Volume / David HESSL in Autism Research, 14-3 (March 2021)  

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Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons / Rong MAO in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

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Enhanced fear limits behavioral flexibility in Shank2-deficient mice / Miru YUN in Molecular Autism, 13 (2022)  

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Overexpression of Homer1a in the basal and lateral amygdala impairs fear conditioning and induces an autism-like social impairment / Anwesha BANERJEE in Molecular Autism, 7 (2016)  

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Reduced electrodermal fear conditioning from ages 3 to 8 years is associated with aggressive behavior at age 8 years / Yu GAO in Journal of Child Psychology and Psychiatry, 51-5 (May 2010)  

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