2016 |
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 |
Under Review
2016 |
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 |