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Björkstrand, Johannes
Publications (10 of 18) Show all publications
Ågren, T., Millroth, P., Andersson, P., Ridzén, M. & Björkstrand, J. (2019). Detailed analysis of skin conductance responses during a gambling task: Decision, anticipation, and outcomes. Psychophysiology, 56(6), Article ID e13338.
Open this publication in new window or tab >>Detailed analysis of skin conductance responses during a gambling task: Decision, anticipation, and outcomes
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2019 (English)In: Psychophysiology, ISSN 0048-5772, E-ISSN 1469-8986, Vol. 56, no 6, article id e13338Article in journal (Refereed) Published
Abstract [en]

Physiological arousal is considered a key factor of gambling behavior. Hence, to understand gambling behavior it is important to study the arousal responses during gambling. Moreover, crucial mechanisms of action could be uncovered by detailing the situations that produce an arousal response. A gamble, or bet, can be partitioned into three distinct phases: (a) decision phase, during which the information concerning the gamble is presented, outcomes are appraised, and a decision is made on how to gamble; (b) anticipation phase, during which the result of the gamble is awaited; (c) outcome phase, during which the outcome of the gamble is presented. Previous research on arousal responses to gambling have mostly measured tonic changes in arousal, and when phasic responses have been measured, analyses have generally concentrated on one of the gamble phases. The aim of the present study was to map the arousal responses during gambling in more detail by measuring skin conductance responses (SCRs) during all three gamble phases of a simple card game. The anticipation phase was found to produce the largest arousal response, suggesting anticipation to be a major contributor to arousal during gambling behavior. Risk behavior during the gambling task was mirrored in self-reported risk taking in everyday life, and risk-takers displayed smaller SCRs compared to nonrisk-takers during decision making, suggesting this as a possible biomarker for risk-taking individuals.

National Category
Psychology (excluding Applied Psychology)
Identifiers
urn:nbn:se:uu:diva-383526 (URN)10.1111/psyp.13338 (DOI)000467437800012 ()30672602 (PubMedID)
Funder
Swedish Research Council
Available from: 2019-05-16 Created: 2019-05-16 Last updated: 2019-06-10Bibliographically approved
Ågren, T., Björkstrand, J. & Fredriksson, M. (2017). Disruption of human fear reconsolidation using imaginal and in vivo extinction. Behavioural Brain Research, 319, 9-15
Open this publication in new window or tab >>Disruption of human fear reconsolidation using imaginal and in vivo extinction
2017 (English)In: Behavioural Brain Research, ISSN 0166-4328, E-ISSN 1872-7549, Vol. 319, p. 9-15Article in journal (Refereed) Published
Abstract [en]

Abstract Memories are not set forever, but can be altered following reactivation, which renders memories malleable, before they are again stabilized through reconsolidation. Fear memories can be attenuated by using extinction during the malleable period. The present study adopts a novel form of extinction, using verbal instructions, in order to examine whether fear memory reconsolidation can be affected by an imaginal exposure. The extinction using verbal instructions, called imaginal extinction, consists of a recorded voice encouraging participants to imagine the scene in which fear was acquired, and to envision the stimuli before their inner eye. The voice signals stimuli appearance, and identical to standard (in vivo) extinction, participants discover that the conditioned stimulus no longer is followed by unconditioned stimulus (UCS). In this way, imaginal extinction translates clinically used imaginal exposure into the standard experimental fear conditioning paradigm. Fear was acquired by pairing pictorial stimuli with an electric shock UCS. Then, both standard and imaginal extinction were given following fear memory reactivation, either after 10 min, within the reconsolidation interval, or after 6 h, outside of the reconsolidation interval. In vivo and imaginal extinction produced comparable reductions in conditioned responses during extinction and importantly, both disrupted reconsolidation of conditioned fear and abolished stimulus discrimination between reinforced and non-reinforced cues. Thus, disrupted reconsolidation of fear conditioning can be achieved without in vivo stimulus presentation, through purely cognitive means, suggesting possible therapeutic applications.

Keywords
Memory reconsolidation, Fear conditioning, Fear extinction, Imaginal exposure, Reinstatement
National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-310376 (URN)10.1016/j.bbr.2016.11.014 (DOI)000392558300002 ()27840245 (PubMedID)
Funder
Swedish Research Council
Available from: 2016-12-14 Created: 2016-12-14 Last updated: 2017-11-29Bibliographically approved
Björkstrand, J. (2017). The Amygdala, Fear and Reconsolidation: Neural and Behavioral Effects of Retrieval-Extinction in Fear Conditioning and Spider Phobia. (Doctoral dissertation). Uppsala: Acta Universitatis Upsaliensis
Open this publication in new window or tab >>The Amygdala, Fear and Reconsolidation: Neural and Behavioral Effects of Retrieval-Extinction in Fear Conditioning and Spider Phobia
2017 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The amygdala is crucially involved in the acquisition and retention of fear memories. Experimental research on fear conditioning has shown that memory retrieval shortly followed by pharmacological manipulations or extinction, thereby interfering with memory reconsolidation, decreases later fear expression. Fear memory reconsolidation depends on synaptic plasticity in the amygdala, which has been demonstrated in rodents using both pharmacological manipulations and retrieval-extinction procedures. The retrieval-extinction procedure decreases fear expression also in humans, but the underlying neural mechanism have not been studied. Interfering with reconsolidation is held to alter the original fear memory representation, resulting in long-term reductions in fear responses, and might therefore be used in the treatment of anxiety disorders, but few studies have directly investigated this question.

The aim of this thesis was to examine the effects of the retrieval-extinction procedure on amygdala activity and behavioral fear expression in humans. The work presented here also investigated whether findings from studies on recent fear memories, established through fear conditioning, extends to naturally occurring long-term phobic fears.

Study I, combining fear conditioning and a retrieval-extinction procedure with functional magnetic resonance imaging (fMRI), demonstrated that memory retrieval shortly followed by extinction reduces later amygdala activity and fear expression in healthy subjects. In Study II, these subjects were re-tested 18 months later. The results showed that the effects on fear expression were still present and that initial amygdala activity predicted long-term fear expression. Using an adapted version of the retrieval-extinction procedure, Study III showed that memory retrieval shortly followed by exposure to spider pictures, attenuates subsequent amygdala activity and increases approach behavior in subjects with life-long fear of spiders. In Study IV, these subjects were re-tested 6 months later, and the results showed that effects on amygdala activity as well as approach behavior were maintained.

In summation, retrieval-extinction leads to long-lasting reductions in amygdala activity and fear expression. These findings are consistent with the hypothesis that retrieval-extinction alters an amygdala dependent fear memory. Retrieval-extinction can also attenuate long-term phobic fears, indicating that this manipulation could be used to enhance exposure-based treatments for anxiety disorders. 

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2017. p. 72
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Social Sciences, ISSN 1652-9030 ; 140
Keywords
Fear conditioning, phobia, memory reconsolidation, retrieval-extinction, exposure therapy, amygdala, fMRI
National Category
Psychology
Research subject
Psychology
Identifiers
urn:nbn:se:uu:diva-317866 (URN)978-91-554-9863-4 (ISBN)
Public defence
2017-05-12, Gunnar Johansson salen, Blåsenhus, von Kraemers allé 1A, Uppsala, 13:00 (English)
Opponent
Supervisors
Available from: 2017-04-20 Created: 2017-03-20 Last updated: 2017-04-20
Björkstrand, J., Ågren, T., Åhs, F., Frick, A., Larsson, E.-M., Hjorth, O., . . . Fredrikson, M. (2017). Think twice, it's all right: Long lasting effects of disrupted reconsolidation on brain and behavior in human long-term fear. Behavioural Brain Research, 324, 125-129
Open this publication in new window or tab >>Think twice, it's all right: Long lasting effects of disrupted reconsolidation on brain and behavior in human long-term fear
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2017 (English)In: Behavioural Brain Research, ISSN 0166-4328, E-ISSN 1872-7549, Vol. 324, p. 125-129Article in journal (Refereed) Published
Abstract [en]

Memories can be modified when recalled. Experimental fear conditioning studies support that amygdala-localized fear memories are attenuated when reconsolidation is disrupted through extinction training immediately following memory activation. Recently, using functional brain imaging in individuals with lifelong spider fears, we demonstrated that fear memory activation followed by repeated exposure to feared cues after 10 min, thereby disrupting reconsolidation, attenuated activity in the amygdala during later re-exposure, and also facilitated approach behavior to feared cues. In contrast, repeated exposure 6 h after fear memory activation, allowing for reconsolidation, did not attenuate amygdala activity and resulted in less approach behavior as compared to the group that received disrupted reconsolidation. We here evaluated if these effects are stable after 6 months and found that amygdala activity was further reduced in both groups, with a tendency towards greater reductions in the 10 min than the 6 h group. Hence, disrupted reconsolidation results in long lasting attenuation of amygdala activity. The behavioral effect, with more approach towards previously feared cues, in the 10 min than the 6 h group also persisted. Thus, the brain effect of disrupted reconsolidation is stable over 6 months and the behavioral effect also remained. We therefore conclude that disrupted reconsolidation result in a long-lasting diminished fear memory representation in the amygdala which may have clinical importance.

Keywords
Reconsolidation disruption, Extinction, Exposure therapy, Amygdala, Approach behavior, Spider fear
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-315854 (URN)10.1016/j.bbr.2017.02.016 (DOI)000397691100016 ()28214541 (PubMedID)
Funder
Swedish Research Council, 2013-2825, 2012-00804The Swedish Brain Foundation, F02014-0151
Available from: 2017-02-21 Created: 2017-02-21 Last updated: 2018-06-26Bibliographically approved
Björkstrand, J., Ågren, T., Frick, A., Engman, J., Larsson, E.-M., Furmark, T. & Fredrikson, M. (2015). Disruption of Memory Reconsolidation Erases a Fear Memory Trace in the Human Amygdala: An 18-Month Follow-Up.. PLoS ONE, 10(7), e0129393
Open this publication in new window or tab >>Disruption of Memory Reconsolidation Erases a Fear Memory Trace in the Human Amygdala: An 18-Month Follow-Up.
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2015 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, no 7, p. e0129393-Article in journal (Refereed) Published
Abstract [en]

Fear memories can be attenuated by reactivation followed by disrupted reconsolidation. Using functional magnetic resonance imaging we recently showed that reactivation and reconsolidation of a conditioned fear memory trace in the basolateral amygdala predicts subsequent fear expression over two days, while reactivation followed by disrupted reconsolidation abolishes the memory trace and suppresses fear. In this follow-up study we demonstrate that the behavioral effect persists over 18 months reflected in superior reacquisition after undisrupted, as compared to disrupted reconsolidation, and that neural activity in the basolateral amygdala representing the initial fear memory predicts return of fear. We conclude that disrupting reconsolidation have long lasting behavioral effects and may permanently erase the fear component of an amygdala-dependent memory.

National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-259785 (URN)10.1371/journal.pone.0129393 (DOI)000358153000028 ()26132145 (PubMedID)
Funder
Swedish Research Council, 521-2010-3284, 421-2009-2343The Swedish Brain Foundation, FO2014-0151
Note

Boethius stiftelse  PSYK2010/143, Swedish Council for Working Life and Social Research, Heumanska stiftelsen

Available from: 2015-08-11 Created: 2015-08-11 Last updated: 2017-12-04Bibliographically approved
Frick, A., Åhs, F., Engman, J., Jonasson, M., Alaie, I., Björkstrand, J., . . . Furmark, T. (2015). Serotonin Synthesis and Reuptake in Social Anxiety Disorder: A Positron Emission Tomography Study.. JAMA psychiatry, 72(8), 794-802
Open this publication in new window or tab >>Serotonin Synthesis and Reuptake in Social Anxiety Disorder: A Positron Emission Tomography Study.
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2015 (English)In: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 72, no 8, p. 794-802Article in journal (Refereed) Published
Abstract [en]

IMPORTANCE: Serotonin is involved in negative affect, but whether anxiety syndromes, such as social anxiety disorder (SAD), are characterized by an overactive or underactive serotonin system has not been established. Serotonin 1A autoreceptors, which inhibit serotonin synthesis and release, are downregulated in SAD, and serotonin transporter availability might be increased; however, presynaptic serotonin activity has not been evaluated extensively.

OBJECTIVE: To examine the serotonin synthesis rate and serotonin transporter availability in patients with SAD and healthy control individuals using positron emission tomography (PET) with the radioligands 5-hydroxytryptophan labeled with carbon 11 ([11C]5-HTP) and 11C-labeled 3-amino-4-(2-dimethylaminomethylphenylsulfanyl)-benzonitrile [11C]DASB.

DESIGN, SETTING, AND PARTICIPANTS: We performed a cross-sectional study at an academic clinical research center. Eighteen patients with SAD (9 men and 9 women; mean [SD] age, 32.6 [8.2] years) and 18 sex- and age-matched healthy controls (9 men and 9 women; mean [SD] age, 34.7 [9.2] years) underwent [11C]5-HTP PET imaging. We acquired [11C]DASB PET images for 26 additional patients with SAD (14 men and 12 women; mean [SD] age, 35.2 [10.7] years) and the same 18 sex- and age-matched healthy controls. Participants were recruited through newspaper advertisements. Data were acquired from March 12, 2002, through March 5, 2012, and analyzed from March 28, 2013, through August 29, 2014.

MAIN OUTCOMES AND MEASURES: The influx rate of [11C]5-HTP as a measure of serotonin synthesis rate capacity and [11C]DASB binding potential as an index of serotonin transporter availability were acquired during rest. We used the Liebowitz Social Anxiety Scale to measure severity of social anxiety symptoms.

RESULTS: The PET data were not available for analysis in 1 control for each scan. Increased [11C]5-HTP influx rate was observed in the amygdala, raphe nuclei region, caudate nucleus, putamen, hippocampus, and anterior cingulate cortex of patients with SAD compared with healthy controls (P < .05 corrected), supporting an enhanced serotonin synthesis rate. Increased serotonin transporter availability in the patients with SAD relative to healthy controls was reflected by elevated [11C]DASB binding potential in the raphe nuclei region, caudate nucleus, putamen, thalamus, and insula cortex (P < .05 corrected).

CONCLUSIONS AND RELEVANCE: Neurotransmission in SAD is characterized by an overactive presynaptic serotonin system, with increased serotonin synthesis and transporter availability. Our findings could provide important new insights into the etiology of anxiety disorders.

National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-259730 (URN)10.1001/jamapsychiatry.2015.0125 (DOI)000359200000008 ()26083190 (PubMedID)
Funder
Swedish Research CouncilThe Swedish Brain FoundationRiksbankens JubileumsfondForte, Swedish Research Council for Health, Working Life and Welfare
Available from: 2015-08-11 Created: 2015-08-11 Last updated: 2017-12-04Bibliographically approved
Engman, J., Frick, A., Alaie, I., Björkstrand, J., Ågren, T., Faria, V., . . . Furmark, T. (2014). Amygdala and Default Mode Network Resting-State Functional Connectivity in Social Anxiety Disorder. In: : . Paper presented at 20th Annual Meeting of the Organization for Human Brain Mapping, Hamburg, Germany, 8-12 juni 2014.
Open this publication in new window or tab >>Amygdala and Default Mode Network Resting-State Functional Connectivity in Social Anxiety Disorder
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2014 (English)Conference paper, Oral presentation only (Refereed)
National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-247730 (URN)
Conference
20th Annual Meeting of the Organization for Human Brain Mapping, Hamburg, Germany, 8-12 juni 2014
Available from: 2015-03-23 Created: 2015-03-23 Last updated: 2015-03-23
Frick, A., Engman, J., Alaie, I., Björkstrand, J., Faria, V., Gingnell, M., . . . Furmark, T. (2014). Enlargement of visual processing regions in social anxiety disorder is related to symptom severity. Neuroscience Letters, 583, 114-119
Open this publication in new window or tab >>Enlargement of visual processing regions in social anxiety disorder is related to symptom severity
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2014 (English)In: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 583, p. 114-119Article in journal (Refereed) Published
Abstract [en]

Social anxiety disorder (SAD) is associated with altered brain function and structure, but most structural studies include small samples and findings are mixed. This study compared regional gray matter volume between 48 SAD patients and 29 healthy controls (HC) as well as the relationship between volume and symptom severity. Structural magnetic resonance images from SAD patients and HC were evaluated using standard voxel-based morphometry (VBM) processing in the SPM8 software package. Social anxiety symptom severity was rated in SAD patients by a clinician using the Liebowitz Social Anxiety Scale (LSAS). SAD patients had greater regional gray matter volume in the lingual gyrus and lateral occipital cortex than the controls, and within the SAD group a positive correlation was found between symptom severity and regional gray matter volume in the lingual gyrus and the retrosplenial cortex. These findings replicate and extend earlier reports of enlarged visual processing areas in SAD. Increased gray matter volume in regions involved in visual processing and self-consciousness could underlie, or be the result of, abnormal emotional information processing and self-focused attention previously demonstrated in patients with SAD.

National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-236363 (URN)10.1016/j.neulet.2014.09.033 (DOI)000345604300022 ()25258347 (PubMedID)
Available from: 2014-11-18 Created: 2014-11-18 Last updated: 2018-01-11Bibliographically approved
Frick, A., Engman, J., Alaie, I., Björkstrand, J., Jonasson, M., Lubberink, M., . . . Furmark, T. (2014). Increased serotonin synthesis and transporter availability in social anxiety disorder revealed by [11C]5-HTP and [11C]DASB PET imaging. In: : . Paper presented at International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Egmond aan Zee, The Netherlands.
Open this publication in new window or tab >>Increased serotonin synthesis and transporter availability in social anxiety disorder revealed by [11C]5-HTP and [11C]DASB PET imaging
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2014 (English)Conference paper, Poster (with or without abstract) (Refereed)
National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-247808 (URN)
Conference
International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Egmond aan Zee, The Netherlands
Available from: 2015-03-24 Created: 2015-03-24 Last updated: 2015-03-24
Frick, A., Engman, J., Alaie, I., Björkstrand, J., Jonasson, M., Lubberink, M., . . . Furmark, T. (2014). Increased serotonin transporter availability in social anxiety disorder revealed by [11C]DASB positron emission tomography. In: : . Paper presented at International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Egmond aan Zee, The Netherlands, 21-24 maj 2014.
Open this publication in new window or tab >>Increased serotonin transporter availability in social anxiety disorder revealed by [11C]DASB positron emission tomography
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2014 (English)Conference paper, Oral presentation only (Refereed)
National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-247673 (URN)
Conference
International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Egmond aan Zee, The Netherlands, 21-24 maj 2014
Available from: 2015-03-23 Created: 2015-03-23 Last updated: 2015-03-23
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