2018 |
Lindström, B; Haaker, J; Olsson, A A common neural network differentially mediates direct and social fear learning Journal Article NeuroImage, 2018. Abstract | Links | BibTeX | Tags: Amygdala, Associability, DCM, Fear conditioning, fMRI, Obsfear procedure, Social learning @article{Lindstr\"{o}m2018, title = {A common neural network differentially mediates direct and social fear learning}, author = {B Lindstr\"{o}m and J Haaker and A Olsson}, doi = {10.1016/j.neuroimage.2017.11.039}, year = {2018}, date = {2018-02-15}, journal = {NeuroImage}, abstract = {Across species, fears often spread between individuals through social learning. Yet, little is known about the neural and computational mechanisms underlying social learning. Addressing this question, we compared social and direct (Pavlovian) fear learning showing that they showed indistinguishable behavioral effects, and involved the same cross-modal (self/other) aversive learning network, centered on the amygdala, the anterior insula (AI), and the anterior cingulate cortex (ACC). Crucially, the information flow within this network differed between social and direct fear learning. Dynamic causal modeling combined with reinforcement learning modeling revealed that the amygdala and AI provided input to this network during direct and social learning, respectively. Furthermore, the AI gated learning signals based on surprise (associability), which were conveyed to the ACC, in both learning modalities. Our findings provide insights into the mechanisms underlying social fear learning, with implications for understanding common psychological dysfunctions, such as phobias and other anxiety disorders.}, keywords = {Amygdala, Associability, DCM, Fear conditioning, fMRI, Obsfear procedure, Social learning}, pubstate = {published}, tppubtype = {article} } Across species, fears often spread between individuals through social learning. Yet, little is known about the neural and computational mechanisms underlying social learning. Addressing this question, we compared social and direct (Pavlovian) fear learning showing that they showed indistinguishable behavioral effects, and involved the same cross-modal (self/other) aversive learning network, centered on the amygdala, the anterior insula (AI), and the anterior cingulate cortex (ACC). Crucially, the information flow within this network differed between social and direct fear learning. Dynamic causal modeling combined with reinforcement learning modeling revealed that the amygdala and AI provided input to this network during direct and social learning, respectively. Furthermore, the AI gated learning signals based on surprise (associability), which were conveyed to the ACC, in both learning modalities. Our findings provide insights into the mechanisms underlying social fear learning, with implications for understanding common psychological dysfunctions, such as phobias and other anxiety disorders. |
2016 |
Haaker, J; Molapour, T; Olsson, A Conditioned social dominance threat: Observation of others' social dominance biases threat learning Journal Article Social Cognitive and Affective Neuroscience, 11 (10), pp. 1627–1637, 2016. Abstract | Links | BibTeX | Tags: Amygdala, Fear extinction, Learning bias, mPFC, Social conflict, Threat-relevance @article{Haaker2016, title = {Conditioned social dominance threat: Observation of others' social dominance biases threat learning}, author = {J Haaker and T Molapour and A Olsson}, url = {http://www.emotionlab.se/wp-content/uploads/2017/10/Haaker-2016-SCAN.pdf}, doi = {10.1093/scan/nsw074}, year = {2016}, date = {2016-10-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {11}, number = {10}, pages = {1627--1637}, abstract = {Social groups are organized along dominance hierarchies, which determine how we respond to threats posed by dominant and subordinate others. The persuasive impact of these dominance threats on mental and physical well-being has been well described but it is unknown how dominance rank of others bias our experience and learning in the first place. We introduce a model of conditioned social dominance threat in humans, where the presence of a dominant other is paired with an aversive event. Participants first learned about the dominance rank of others by observing their dyadic confrontations. During subsequent fear learning, the dominant and subordinate others were equally predictive of an aversive consequence (mild electric shock) to the participant. In three separate experiments, we show that participants' eye-blink startle responses and amygdala reactivity adaptively tracked dominance of others during observation of confrontation. Importantly, during fear learning dominant vs subordinate others elicited stronger and more persistent learned threat responses as measured by physiological arousal and amygdala activity. Our results characterize the neural basis of learning through observing conflicts between others, and how this affects subsequent learning through direct, personal experiences.}, keywords = {Amygdala, Fear extinction, Learning bias, mPFC, Social conflict, Threat-relevance}, pubstate = {published}, tppubtype = {article} } Social groups are organized along dominance hierarchies, which determine how we respond to threats posed by dominant and subordinate others. The persuasive impact of these dominance threats on mental and physical well-being has been well described but it is unknown how dominance rank of others bias our experience and learning in the first place. We introduce a model of conditioned social dominance threat in humans, where the presence of a dominant other is paired with an aversive event. Participants first learned about the dominance rank of others by observing their dyadic confrontations. During subsequent fear learning, the dominant and subordinate others were equally predictive of an aversive consequence (mild electric shock) to the participant. In three separate experiments, we show that participants' eye-blink startle responses and amygdala reactivity adaptively tracked dominance of others during observation of confrontation. Importantly, during fear learning dominant vs subordinate others elicited stronger and more persistent learned threat responses as measured by physiological arousal and amygdala activity. Our results characterize the neural basis of learning through observing conflicts between others, and how this affects subsequent learning through direct, personal experiences. |
Golkar, A; Haaker, J; Selbing, I; Olsson, A Neural signals of vicarious extinction learning Journal Article Social Cognitive and Affective Neuroscience, 11 (10), pp. 1541-1549, 2016. Abstract | Links | BibTeX | Tags: Amygdala, Extinction, Obsfear procedure, Social learning, Vicarious learning, vmPFC @article{Golkar2016, title = {Neural signals of vicarious extinction learning}, author = {A Golkar and J Haaker and I Selbing and A Olsson}, url = {http://www.emotionlab.se/wp-content/uploads/2017/02/Armita_SCAN_authorscopy.pdf}, doi = {10.1093/scan/nsw068}, year = {2016}, date = {2016-02-13}, journal = {Social Cognitive and Affective Neuroscience}, volume = {11}, number = {10}, pages = {1541-1549}, abstract = {Social transmission of both threat and safety is ubiquitous, but little is known about the neural circuitry underlying vicarious safety learning. This is surprising given that these processes are critical to flexibly adapt to a changeable environment. To address how the expression of previously learned fears can be modified by the transmission of social information, two conditioned stimuli (CS + s) were paired with shock and the third was not. During extinction, we held constant the amount of direct, non-reinforced, exposure to the CSs (i.e. direct extinction), and critically varied whether another individual-acting as a demonstrator-experienced safety (CS + vic safety) or aversive reinforcement (CS + vic reinf). During extinction, ventromedial prefrontal cortex (vmPFC) responses to the CS + vic reinf increased but decreased to the CS + vic safety This pattern of vmPFC activity was reversed during a subsequent fear reinstatement test, suggesting a temporal shift in the involvement of the vmPFC. Moreover, only the CS + vic reinf association recovered. Our data suggest that vicarious extinction prevents the return of conditioned fear responses, and that this efficacy is reflected by diminished vmPFC involvement during extinction learning. The present findings may have important implications for understanding how social information influences the persistence of fear memories in individuals suffering from emotional disorders.}, keywords = {Amygdala, Extinction, Obsfear procedure, Social learning, Vicarious learning, vmPFC}, pubstate = {published}, tppubtype = {article} } Social transmission of both threat and safety is ubiquitous, but little is known about the neural circuitry underlying vicarious safety learning. This is surprising given that these processes are critical to flexibly adapt to a changeable environment. To address how the expression of previously learned fears can be modified by the transmission of social information, two conditioned stimuli (CS + s) were paired with shock and the third was not. During extinction, we held constant the amount of direct, non-reinforced, exposure to the CSs (i.e. direct extinction), and critically varied whether another individual-acting as a demonstrator-experienced safety (CS + vic safety) or aversive reinforcement (CS + vic reinf). During extinction, ventromedial prefrontal cortex (vmPFC) responses to the CS + vic reinf increased but decreased to the CS + vic safety This pattern of vmPFC activity was reversed during a subsequent fear reinstatement test, suggesting a temporal shift in the involvement of the vmPFC. Moreover, only the CS + vic reinf association recovered. Our data suggest that vicarious extinction prevents the return of conditioned fear responses, and that this efficacy is reflected by diminished vmPFC involvement during extinction learning. The present findings may have important implications for understanding how social information influences the persistence of fear memories in individuals suffering from emotional disorders. |
2015 |
Lonsdorf, T B; Golkar, A; Lindström, K M; Haaker, J; Öhman, A; Schalling, M; Ingvar, M BDNF val66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall Journal Article Social Cognitive and Affective Neuroscience, 10 (5), pp. 664–671, 2015, ISSN: 1749-5016. Abstract | Links | BibTeX | Tags: Amygdala, Anxiety, CBT, Fear recall, Therapygenetics, vmPFC @article{Lonsdorf2015, title = {BDNF val66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall}, author = {T B Lonsdorf and A Golkar and K M Lindstr\"{o}m and J Haaker and A \"{O}hman and M Schalling and M Ingvar}, url = {http://www.emotionlab.se/wp-content/uploads/2017/10/Lonsdorf_BDNFval66met_2014.pdf}, doi = {10.1093/scan/nsu102}, issn = {1749-5016}, year = {2015}, date = {2015-05-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {10}, number = {5}, pages = {664--671}, abstract = {Brain-derived neurotrophic factor (BDNF), the most abundant neutrophin in the mammalian central nervous system, is critically involved in synaptic plasticity. In both rodents and humans, BDNF has been implicated in hippocampus- and amygdala-dependent learning and memory and has more recently been linked to fear extinction processes. Fifty-nine healthy participants, genotyped for the functional BDNFval66met polymorphism, underwent a fear conditioning and 24h-delayed extinction protocol while skin conductance and blood oxygenation level dependent (BOLD) responses (functional magnetic resonance imaging) were acquired. We present the first report of neural activation pattern during fear acquisition and extinction for the BDNFval66met polymorphism using a differential conditioned stimulus (CS)þ textgreater CS comparison. During conditioning, we observed heightened allele dose-dependent responses in the amygdala and reduced responses in the subgenual anterior cingulate cortex in BDNFval66met met-carriers. During early extinction, 24h later, we again observed heightened responses in several regions ascribed to the fear network in met-carriers as opposed to valcarriers (insula, amygdala, hippocampus), which likely reflects fear memory recall. No differences were observed during late extinction, which likely reflects learned extinction. Our data thus support previous associations of the BDNFval66met polymorphism with neural activation in the fear and extinction network, but speak against a specific association with fear extinction processes. K}, keywords = {Amygdala, Anxiety, CBT, Fear recall, Therapygenetics, vmPFC}, pubstate = {published}, tppubtype = {article} } Brain-derived neurotrophic factor (BDNF), the most abundant neutrophin in the mammalian central nervous system, is critically involved in synaptic plasticity. In both rodents and humans, BDNF has been implicated in hippocampus- and amygdala-dependent learning and memory and has more recently been linked to fear extinction processes. Fifty-nine healthy participants, genotyped for the functional BDNFval66met polymorphism, underwent a fear conditioning and 24h-delayed extinction protocol while skin conductance and blood oxygenation level dependent (BOLD) responses (functional magnetic resonance imaging) were acquired. We present the first report of neural activation pattern during fear acquisition and extinction for the BDNFval66met polymorphism using a differential conditioned stimulus (CS)þ textgreater CS comparison. During conditioning, we observed heightened allele dose-dependent responses in the amygdala and reduced responses in the subgenual anterior cingulate cortex in BDNFval66met met-carriers. During early extinction, 24h later, we again observed heightened responses in several regions ascribed to the fear network in met-carriers as opposed to valcarriers (insula, amygdala, hippocampus), which likely reflects fear memory recall. No differences were observed during late extinction, which likely reflects learned extinction. Our data thus support previous associations of the BDNFval66met polymorphism with neural activation in the fear and extinction network, but speak against a specific association with fear extinction processes. K |
2007 |
Öhman, A; Carlsson, K; Lundqvist, D; Ingvar, M On the unconscious subcortical origin of human fear Journal Article Physiology & Behavior, 92 (1-2), pp. 180–185, 2007, ISSN: 00319384. Abstract | Links | BibTeX | Tags: Amygdala, Backward masking, Evolution, Fear, Subcortex @article{Ohman2007a, title = {On the unconscious subcortical origin of human fear}, author = {A \"{O}hman and K Carlsson and D Lundqvist and M Ingvar}, doi = {10.1016/j.physbeh.2007.05.057}, issn = {00319384}, year = {2007}, date = {2007-09-01}, journal = {Physiology & Behavior}, volume = {92}, number = {1-2}, pages = {180--185}, abstract = {Consistent with the hypothesis that the amygdala is central to fear activation, brain imaging studies show that fear stimuli activate the amygdala, even when conscious recognition is prevented by backward masking. The bulk of the data suggest that the amygdala can be activated from potentially accessible but unattended fear stimuli. Activation of the amygdala facilitates low level visual processing. Several lines of evidence suggest that activation of the amygdala is mediated by a subcortical pathway. Thus, according to data from patients with lesions in the primary visual cortex, the amygdala can be activated in the absence of cortical processing. There is considerable support for the hypothesis that visual stimuli can access the amygdala via a pathway that includes the superior colliculus and the pulvinar nucleus of the thalamus. These data are consistent with an evolutionary argument, focusing of the role of snakes as a predator on primates.}, keywords = {Amygdala, Backward masking, Evolution, Fear, Subcortex}, pubstate = {published}, tppubtype = {article} } Consistent with the hypothesis that the amygdala is central to fear activation, brain imaging studies show that fear stimuli activate the amygdala, even when conscious recognition is prevented by backward masking. The bulk of the data suggest that the amygdala can be activated from potentially accessible but unattended fear stimuli. Activation of the amygdala facilitates low level visual processing. Several lines of evidence suggest that activation of the amygdala is mediated by a subcortical pathway. Thus, according to data from patients with lesions in the primary visual cortex, the amygdala can be activated in the absence of cortical processing. There is considerable support for the hypothesis that visual stimuli can access the amygdala via a pathway that includes the superior colliculus and the pulvinar nucleus of the thalamus. These data are consistent with an evolutionary argument, focusing of the role of snakes as a predator on primates. |
Olsson, A; Nearing, K I; Phelps, E A Learning fears by observing others: the neural systems of social fear transmission Journal Article Social Cognitive and Affective Neuroscience, 2 (1), pp. 3–11, 2007, ISSN: 1749-5016. Abstract | Links | BibTeX | Tags: Amygdala, Empathy, Fear conditioning, fMRI, Obsfear procedure, Social learning @article{Olsson2007a, title = {Learning fears by observing others: the neural systems of social fear transmission}, author = {A Olsson and K I Nearing and E A Phelps}, doi = {10.1093/scan/nsm005}, issn = {1749-5016}, year = {2007}, date = {2007-03-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {2}, number = {1}, pages = {3--11}, abstract = {Classical fear conditioning has been used as a model paradigm to explain fear learning across species. In this paradigm, the amygdala is known to play a critical role. However, classical fear conditioning requires first-hand experience with an aversive event, which may not be how most fears are acquired in humans. It remains to be determined whether the conditioning model can be extended to indirect forms of learning more common in humans. Here we show that fear acquired indirectly through social observation, with no personal experience of the aversive event, engages similar neural mechanisms as fear conditioning. The amygdala was recruited both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in an analogous situation. These findings confirm the central role of the amygdala in the acquisition and expression of observational fear learning, and validate the extension of cross-species models of fear conditioning to learning in a human sociocultural context. Our findings also provides new insights into the relationship between learning from, and empathizing with, fearful others. This study suggests that indirectly attained fears may be as powerful as fears originating from direct experiences.}, keywords = {Amygdala, Empathy, Fear conditioning, fMRI, Obsfear procedure, Social learning}, pubstate = {published}, tppubtype = {article} } Classical fear conditioning has been used as a model paradigm to explain fear learning across species. In this paradigm, the amygdala is known to play a critical role. However, classical fear conditioning requires first-hand experience with an aversive event, which may not be how most fears are acquired in humans. It remains to be determined whether the conditioning model can be extended to indirect forms of learning more common in humans. Here we show that fear acquired indirectly through social observation, with no personal experience of the aversive event, engages similar neural mechanisms as fear conditioning. The amygdala was recruited both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in an analogous situation. These findings confirm the central role of the amygdala in the acquisition and expression of observational fear learning, and validate the extension of cross-species models of fear conditioning to learning in a human sociocultural context. Our findings also provides new insights into the relationship between learning from, and empathizing with, fearful others. This study suggests that indirectly attained fears may be as powerful as fears originating from direct experiences. |
2006 |
Delgado, M R; Olsson, A; Phelps, E A Extending animal models of fear conditioning to humans Journal Article Biological Psychology, 73 (1), pp. 39–48, 2006, ISSN: 03010511. Abstract | Links | BibTeX | Tags: Acquisition, Amygdala, Anxiety disorders, Emotion, Emotion regulation, Extinction, Infralimbic, Learning, Prefrontal cortex, Prelimbic @article{Delgado2006, title = {Extending animal models of fear conditioning to humans}, author = {M R Delgado and A Olsson and E A Phelps}, doi = {10.1016/j.biopsycho.2006.01.006}, issn = {03010511}, year = {2006}, date = {2006-07-01}, journal = {Biological Psychology}, volume = {73}, number = {1}, pages = {39--48}, abstract = {A goal of fear and anxiety research is to understand how to treat the potentially devastating effects of anxiety disorders in humans. Much of this research utilizes classical fear conditioning, a simple paradigm that has been extensively investigated in animals, helping outline a brain circuitry thought to be responsible for the acquisition, expression and extinction of fear. The findings from non-human animal research have more recently been substantiated and extended in humans, using neuropsychological and neuroimaging methodologies. Research across species concur that the neural correlates of fear conditioning include involvement of the amygdala during all stages of fear learning, and prefrontal areas during the extinction phase. This manuscript reviews how animal models of fear are translated to human behavior, and how some fears are more easily acquired in humans (i.e., social\textendashcultural). Finally, using the knowledge provided by a rich animal literature, we attempt to extend these findings to human models targeted to helping facilitate extinction or abolishment of fears, a trademark of anxiety disorders, by discussing efficacy in modulating the brain circuitry involved in fear conditioning via pharmacological treatments or emotion regulation cognitive strategies.}, keywords = {Acquisition, Amygdala, Anxiety disorders, Emotion, Emotion regulation, Extinction, Infralimbic, Learning, Prefrontal cortex, Prelimbic}, pubstate = {published}, tppubtype = {article} } A goal of fear and anxiety research is to understand how to treat the potentially devastating effects of anxiety disorders in humans. Much of this research utilizes classical fear conditioning, a simple paradigm that has been extensively investigated in animals, helping outline a brain circuitry thought to be responsible for the acquisition, expression and extinction of fear. The findings from non-human animal research have more recently been substantiated and extended in humans, using neuropsychological and neuroimaging methodologies. Research across species concur that the neural correlates of fear conditioning include involvement of the amygdala during all stages of fear learning, and prefrontal areas during the extinction phase. This manuscript reviews how animal models of fear are translated to human behavior, and how some fears are more easily acquired in humans (i.e., social–cultural). Finally, using the knowledge provided by a rich animal literature, we attempt to extend these findings to human models targeted to helping facilitate extinction or abolishment of fears, a trademark of anxiety disorders, by discussing efficacy in modulating the brain circuitry involved in fear conditioning via pharmacological treatments or emotion regulation cognitive strategies. |
Under Review
2018 |
Lindström, B; Haaker, J; Olsson, A A common neural network differentially mediates direct and social fear learning Journal Article NeuroImage, 2018. @article{Lindstr\"{o}m2018, title = {A common neural network differentially mediates direct and social fear learning}, author = {B Lindstr\"{o}m and J Haaker and A Olsson}, doi = {10.1016/j.neuroimage.2017.11.039}, year = {2018}, date = {2018-02-15}, journal = {NeuroImage}, abstract = {Across species, fears often spread between individuals through social learning. Yet, little is known about the neural and computational mechanisms underlying social learning. Addressing this question, we compared social and direct (Pavlovian) fear learning showing that they showed indistinguishable behavioral effects, and involved the same cross-modal (self/other) aversive learning network, centered on the amygdala, the anterior insula (AI), and the anterior cingulate cortex (ACC). Crucially, the information flow within this network differed between social and direct fear learning. Dynamic causal modeling combined with reinforcement learning modeling revealed that the amygdala and AI provided input to this network during direct and social learning, respectively. Furthermore, the AI gated learning signals based on surprise (associability), which were conveyed to the ACC, in both learning modalities. Our findings provide insights into the mechanisms underlying social fear learning, with implications for understanding common psychological dysfunctions, such as phobias and other anxiety disorders.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Across species, fears often spread between individuals through social learning. Yet, little is known about the neural and computational mechanisms underlying social learning. Addressing this question, we compared social and direct (Pavlovian) fear learning showing that they showed indistinguishable behavioral effects, and involved the same cross-modal (self/other) aversive learning network, centered on the amygdala, the anterior insula (AI), and the anterior cingulate cortex (ACC). Crucially, the information flow within this network differed between social and direct fear learning. Dynamic causal modeling combined with reinforcement learning modeling revealed that the amygdala and AI provided input to this network during direct and social learning, respectively. Furthermore, the AI gated learning signals based on surprise (associability), which were conveyed to the ACC, in both learning modalities. Our findings provide insights into the mechanisms underlying social fear learning, with implications for understanding common psychological dysfunctions, such as phobias and other anxiety disorders. |
2016 |
Haaker, J; Molapour, T; Olsson, A Conditioned social dominance threat: Observation of others' social dominance biases threat learning Journal Article Social Cognitive and Affective Neuroscience, 11 (10), pp. 1627–1637, 2016. @article{Haaker2016, title = {Conditioned social dominance threat: Observation of others' social dominance biases threat learning}, author = {J Haaker and T Molapour and A Olsson}, url = {http://www.emotionlab.se/wp-content/uploads/2017/10/Haaker-2016-SCAN.pdf}, doi = {10.1093/scan/nsw074}, year = {2016}, date = {2016-10-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {11}, number = {10}, pages = {1627--1637}, abstract = {Social groups are organized along dominance hierarchies, which determine how we respond to threats posed by dominant and subordinate others. The persuasive impact of these dominance threats on mental and physical well-being has been well described but it is unknown how dominance rank of others bias our experience and learning in the first place. We introduce a model of conditioned social dominance threat in humans, where the presence of a dominant other is paired with an aversive event. Participants first learned about the dominance rank of others by observing their dyadic confrontations. During subsequent fear learning, the dominant and subordinate others were equally predictive of an aversive consequence (mild electric shock) to the participant. In three separate experiments, we show that participants' eye-blink startle responses and amygdala reactivity adaptively tracked dominance of others during observation of confrontation. Importantly, during fear learning dominant vs subordinate others elicited stronger and more persistent learned threat responses as measured by physiological arousal and amygdala activity. Our results characterize the neural basis of learning through observing conflicts between others, and how this affects subsequent learning through direct, personal experiences.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Social groups are organized along dominance hierarchies, which determine how we respond to threats posed by dominant and subordinate others. The persuasive impact of these dominance threats on mental and physical well-being has been well described but it is unknown how dominance rank of others bias our experience and learning in the first place. We introduce a model of conditioned social dominance threat in humans, where the presence of a dominant other is paired with an aversive event. Participants first learned about the dominance rank of others by observing their dyadic confrontations. During subsequent fear learning, the dominant and subordinate others were equally predictive of an aversive consequence (mild electric shock) to the participant. In three separate experiments, we show that participants' eye-blink startle responses and amygdala reactivity adaptively tracked dominance of others during observation of confrontation. Importantly, during fear learning dominant vs subordinate others elicited stronger and more persistent learned threat responses as measured by physiological arousal and amygdala activity. Our results characterize the neural basis of learning through observing conflicts between others, and how this affects subsequent learning through direct, personal experiences. |
Golkar, A; Haaker, J; Selbing, I; Olsson, A Neural signals of vicarious extinction learning Journal Article Social Cognitive and Affective Neuroscience, 11 (10), pp. 1541-1549, 2016. @article{Golkar2016, title = {Neural signals of vicarious extinction learning}, author = {A Golkar and J Haaker and I Selbing and A Olsson}, url = {http://www.emotionlab.se/wp-content/uploads/2017/02/Armita_SCAN_authorscopy.pdf}, doi = {10.1093/scan/nsw068}, year = {2016}, date = {2016-02-13}, journal = {Social Cognitive and Affective Neuroscience}, volume = {11}, number = {10}, pages = {1541-1549}, abstract = {Social transmission of both threat and safety is ubiquitous, but little is known about the neural circuitry underlying vicarious safety learning. This is surprising given that these processes are critical to flexibly adapt to a changeable environment. To address how the expression of previously learned fears can be modified by the transmission of social information, two conditioned stimuli (CS + s) were paired with shock and the third was not. During extinction, we held constant the amount of direct, non-reinforced, exposure to the CSs (i.e. direct extinction), and critically varied whether another individual-acting as a demonstrator-experienced safety (CS + vic safety) or aversive reinforcement (CS + vic reinf). During extinction, ventromedial prefrontal cortex (vmPFC) responses to the CS + vic reinf increased but decreased to the CS + vic safety This pattern of vmPFC activity was reversed during a subsequent fear reinstatement test, suggesting a temporal shift in the involvement of the vmPFC. Moreover, only the CS + vic reinf association recovered. Our data suggest that vicarious extinction prevents the return of conditioned fear responses, and that this efficacy is reflected by diminished vmPFC involvement during extinction learning. The present findings may have important implications for understanding how social information influences the persistence of fear memories in individuals suffering from emotional disorders.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Social transmission of both threat and safety is ubiquitous, but little is known about the neural circuitry underlying vicarious safety learning. This is surprising given that these processes are critical to flexibly adapt to a changeable environment. To address how the expression of previously learned fears can be modified by the transmission of social information, two conditioned stimuli (CS + s) were paired with shock and the third was not. During extinction, we held constant the amount of direct, non-reinforced, exposure to the CSs (i.e. direct extinction), and critically varied whether another individual-acting as a demonstrator-experienced safety (CS + vic safety) or aversive reinforcement (CS + vic reinf). During extinction, ventromedial prefrontal cortex (vmPFC) responses to the CS + vic reinf increased but decreased to the CS + vic safety This pattern of vmPFC activity was reversed during a subsequent fear reinstatement test, suggesting a temporal shift in the involvement of the vmPFC. Moreover, only the CS + vic reinf association recovered. Our data suggest that vicarious extinction prevents the return of conditioned fear responses, and that this efficacy is reflected by diminished vmPFC involvement during extinction learning. The present findings may have important implications for understanding how social information influences the persistence of fear memories in individuals suffering from emotional disorders. |
2015 |
Lonsdorf, T B; Golkar, A; Lindström, K M; Haaker, J; Öhman, A; Schalling, M; Ingvar, M BDNF val66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall Journal Article Social Cognitive and Affective Neuroscience, 10 (5), pp. 664–671, 2015, ISSN: 1749-5016. @article{Lonsdorf2015, title = {BDNF val66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall}, author = {T B Lonsdorf and A Golkar and K M Lindstr\"{o}m and J Haaker and A \"{O}hman and M Schalling and M Ingvar}, url = {http://www.emotionlab.se/wp-content/uploads/2017/10/Lonsdorf_BDNFval66met_2014.pdf}, doi = {10.1093/scan/nsu102}, issn = {1749-5016}, year = {2015}, date = {2015-05-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {10}, number = {5}, pages = {664--671}, abstract = {Brain-derived neurotrophic factor (BDNF), the most abundant neutrophin in the mammalian central nervous system, is critically involved in synaptic plasticity. In both rodents and humans, BDNF has been implicated in hippocampus- and amygdala-dependent learning and memory and has more recently been linked to fear extinction processes. Fifty-nine healthy participants, genotyped for the functional BDNFval66met polymorphism, underwent a fear conditioning and 24h-delayed extinction protocol while skin conductance and blood oxygenation level dependent (BOLD) responses (functional magnetic resonance imaging) were acquired. We present the first report of neural activation pattern during fear acquisition and extinction for the BDNFval66met polymorphism using a differential conditioned stimulus (CS)þ textgreater CS comparison. During conditioning, we observed heightened allele dose-dependent responses in the amygdala and reduced responses in the subgenual anterior cingulate cortex in BDNFval66met met-carriers. During early extinction, 24h later, we again observed heightened responses in several regions ascribed to the fear network in met-carriers as opposed to valcarriers (insula, amygdala, hippocampus), which likely reflects fear memory recall. No differences were observed during late extinction, which likely reflects learned extinction. Our data thus support previous associations of the BDNFval66met polymorphism with neural activation in the fear and extinction network, but speak against a specific association with fear extinction processes. K}, keywords = {}, pubstate = {published}, tppubtype = {article} } Brain-derived neurotrophic factor (BDNF), the most abundant neutrophin in the mammalian central nervous system, is critically involved in synaptic plasticity. In both rodents and humans, BDNF has been implicated in hippocampus- and amygdala-dependent learning and memory and has more recently been linked to fear extinction processes. Fifty-nine healthy participants, genotyped for the functional BDNFval66met polymorphism, underwent a fear conditioning and 24h-delayed extinction protocol while skin conductance and blood oxygenation level dependent (BOLD) responses (functional magnetic resonance imaging) were acquired. We present the first report of neural activation pattern during fear acquisition and extinction for the BDNFval66met polymorphism using a differential conditioned stimulus (CS)þ textgreater CS comparison. During conditioning, we observed heightened allele dose-dependent responses in the amygdala and reduced responses in the subgenual anterior cingulate cortex in BDNFval66met met-carriers. During early extinction, 24h later, we again observed heightened responses in several regions ascribed to the fear network in met-carriers as opposed to valcarriers (insula, amygdala, hippocampus), which likely reflects fear memory recall. No differences were observed during late extinction, which likely reflects learned extinction. Our data thus support previous associations of the BDNFval66met polymorphism with neural activation in the fear and extinction network, but speak against a specific association with fear extinction processes. K |
2007 |
Öhman, A; Carlsson, K; Lundqvist, D; Ingvar, M On the unconscious subcortical origin of human fear Journal Article Physiology & Behavior, 92 (1-2), pp. 180–185, 2007, ISSN: 00319384. @article{Ohman2007a, title = {On the unconscious subcortical origin of human fear}, author = {A \"{O}hman and K Carlsson and D Lundqvist and M Ingvar}, doi = {10.1016/j.physbeh.2007.05.057}, issn = {00319384}, year = {2007}, date = {2007-09-01}, journal = {Physiology & Behavior}, volume = {92}, number = {1-2}, pages = {180--185}, abstract = {Consistent with the hypothesis that the amygdala is central to fear activation, brain imaging studies show that fear stimuli activate the amygdala, even when conscious recognition is prevented by backward masking. The bulk of the data suggest that the amygdala can be activated from potentially accessible but unattended fear stimuli. Activation of the amygdala facilitates low level visual processing. Several lines of evidence suggest that activation of the amygdala is mediated by a subcortical pathway. Thus, according to data from patients with lesions in the primary visual cortex, the amygdala can be activated in the absence of cortical processing. There is considerable support for the hypothesis that visual stimuli can access the amygdala via a pathway that includes the superior colliculus and the pulvinar nucleus of the thalamus. These data are consistent with an evolutionary argument, focusing of the role of snakes as a predator on primates.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Consistent with the hypothesis that the amygdala is central to fear activation, brain imaging studies show that fear stimuli activate the amygdala, even when conscious recognition is prevented by backward masking. The bulk of the data suggest that the amygdala can be activated from potentially accessible but unattended fear stimuli. Activation of the amygdala facilitates low level visual processing. Several lines of evidence suggest that activation of the amygdala is mediated by a subcortical pathway. Thus, according to data from patients with lesions in the primary visual cortex, the amygdala can be activated in the absence of cortical processing. There is considerable support for the hypothesis that visual stimuli can access the amygdala via a pathway that includes the superior colliculus and the pulvinar nucleus of the thalamus. These data are consistent with an evolutionary argument, focusing of the role of snakes as a predator on primates. |
Olsson, A; Nearing, K I; Phelps, E A Learning fears by observing others: the neural systems of social fear transmission Journal Article Social Cognitive and Affective Neuroscience, 2 (1), pp. 3–11, 2007, ISSN: 1749-5016. @article{Olsson2007a, title = {Learning fears by observing others: the neural systems of social fear transmission}, author = {A Olsson and K I Nearing and E A Phelps}, doi = {10.1093/scan/nsm005}, issn = {1749-5016}, year = {2007}, date = {2007-03-01}, journal = {Social Cognitive and Affective Neuroscience}, volume = {2}, number = {1}, pages = {3--11}, abstract = {Classical fear conditioning has been used as a model paradigm to explain fear learning across species. In this paradigm, the amygdala is known to play a critical role. However, classical fear conditioning requires first-hand experience with an aversive event, which may not be how most fears are acquired in humans. It remains to be determined whether the conditioning model can be extended to indirect forms of learning more common in humans. Here we show that fear acquired indirectly through social observation, with no personal experience of the aversive event, engages similar neural mechanisms as fear conditioning. The amygdala was recruited both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in an analogous situation. These findings confirm the central role of the amygdala in the acquisition and expression of observational fear learning, and validate the extension of cross-species models of fear conditioning to learning in a human sociocultural context. Our findings also provides new insights into the relationship between learning from, and empathizing with, fearful others. This study suggests that indirectly attained fears may be as powerful as fears originating from direct experiences.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Classical fear conditioning has been used as a model paradigm to explain fear learning across species. In this paradigm, the amygdala is known to play a critical role. However, classical fear conditioning requires first-hand experience with an aversive event, which may not be how most fears are acquired in humans. It remains to be determined whether the conditioning model can be extended to indirect forms of learning more common in humans. Here we show that fear acquired indirectly through social observation, with no personal experience of the aversive event, engages similar neural mechanisms as fear conditioning. The amygdala was recruited both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in an analogous situation. These findings confirm the central role of the amygdala in the acquisition and expression of observational fear learning, and validate the extension of cross-species models of fear conditioning to learning in a human sociocultural context. Our findings also provides new insights into the relationship between learning from, and empathizing with, fearful others. This study suggests that indirectly attained fears may be as powerful as fears originating from direct experiences. |
2006 |
Delgado, M R; Olsson, A; Phelps, E A Extending animal models of fear conditioning to humans Journal Article Biological Psychology, 73 (1), pp. 39–48, 2006, ISSN: 03010511. @article{Delgado2006, title = {Extending animal models of fear conditioning to humans}, author = {M R Delgado and A Olsson and E A Phelps}, doi = {10.1016/j.biopsycho.2006.01.006}, issn = {03010511}, year = {2006}, date = {2006-07-01}, journal = {Biological Psychology}, volume = {73}, number = {1}, pages = {39--48}, abstract = {A goal of fear and anxiety research is to understand how to treat the potentially devastating effects of anxiety disorders in humans. Much of this research utilizes classical fear conditioning, a simple paradigm that has been extensively investigated in animals, helping outline a brain circuitry thought to be responsible for the acquisition, expression and extinction of fear. The findings from non-human animal research have more recently been substantiated and extended in humans, using neuropsychological and neuroimaging methodologies. Research across species concur that the neural correlates of fear conditioning include involvement of the amygdala during all stages of fear learning, and prefrontal areas during the extinction phase. This manuscript reviews how animal models of fear are translated to human behavior, and how some fears are more easily acquired in humans (i.e., social\textendashcultural). Finally, using the knowledge provided by a rich animal literature, we attempt to extend these findings to human models targeted to helping facilitate extinction or abolishment of fears, a trademark of anxiety disorders, by discussing efficacy in modulating the brain circuitry involved in fear conditioning via pharmacological treatments or emotion regulation cognitive strategies.}, keywords = {}, pubstate = {published}, tppubtype = {article} } A goal of fear and anxiety research is to understand how to treat the potentially devastating effects of anxiety disorders in humans. Much of this research utilizes classical fear conditioning, a simple paradigm that has been extensively investigated in animals, helping outline a brain circuitry thought to be responsible for the acquisition, expression and extinction of fear. The findings from non-human animal research have more recently been substantiated and extended in humans, using neuropsychological and neuroimaging methodologies. Research across species concur that the neural correlates of fear conditioning include involvement of the amygdala during all stages of fear learning, and prefrontal areas during the extinction phase. This manuscript reviews how animal models of fear are translated to human behavior, and how some fears are more easily acquired in humans (i.e., social–cultural). Finally, using the knowledge provided by a rich animal literature, we attempt to extend these findings to human models targeted to helping facilitate extinction or abolishment of fears, a trademark of anxiety disorders, by discussing efficacy in modulating the brain circuitry involved in fear conditioning via pharmacological treatments or emotion regulation cognitive strategies. |