Dataset Information

BDNFval66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall.

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)+ > 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 val-carriers (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.

SUBMITTER: Lonsdorf TB

PROVIDER: S-EPMC4420743 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

BDNFval66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall.

Lonsdorf Tina B TB Golkar Armita A Lindström Kara M KM Haaker Jan J Öhman Arne A Schalling Martin M Ingvar Martin M

Social cognitive and affective neuroscience 20140807 5

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 ...[more]

PMID: 25103087

Similar Datasets

Project description:The fear conditioning and extinction neurocircuitry has been extensively studied in healthy and clinical populations, with a particular focus on posttraumatic stress disorder. Despite significant overlap of symptoms between posttraumatic stress disorder and anxiety disorders, the latter has received less attention. Given that dysregulated fear levels characterize anxiety disorders, examining the neural correlates of fear and extinction learning may shed light on the pathogenesis of underlying anxiety disorders.To investigate the psychophysiological and neural correlates of fear conditioning and extinction recall in anxiety disorders and to document how these features differ as a function of multiple diagnoses or anxiety severity.This investigation was a cross-sectional, case-control, functional magnetic resonance imaging study at an academic medical center. Participants were healthy controls and individuals with at least 1 of the following anxiety disorders: generalized anxiety disorder, social anxiety disorder, specific phobia, and panic disorder. The study dates were between March 2013 and May 2015.Two-day fear conditioning and extinction paradigm.Skin conductance responses, blood oxygenation level-dependent responses, trait anxiety scores from the State Trait Anxiety Inventory-Trait Form, and functional connectivity.This study included 21 healthy controls (10 women) and 61 individuals with anxiety disorders (36 women). P values reported for the neuroimaging results are all familywise error corrected. Skin conductance responses during extinction recall did not differ between individuals with anxiety disorders and healthy controls (?p2?=?0.001, P?=?.79), where ?p2 is partial eta squared. The anxiety group had lower activation of the ventromedial prefrontal cortex (vmPFC) during extinction recall (?p2?=?0.178, P?=?.02). A similar hypoactive pattern was found during early conditioning (?p2?=?0.106, P?=?.009). The vmPFC hypoactivation was associated with anxiety symptom severity (r?=?-0.420, P?=?.01 for conditioning and r?=?-0.464, P?=?.004 for extinction recall) and the number of co-occuring anxiety disorders diagnosed (?p2?=?0.137, P?=?.009 for conditioning and ?p2?=?0.227, P?=?.004 for extinction recall). Psychophysiological interaction analyses revealed that the fear network connectivity differed between healthy controls and the anxiety group during fear learning (?p2 range between 0.088 and 0.176 and P range between 0.02 and 0.003) and extinction recall (?p2 range between 0.111 and 0.235 and P range between 0.02 and 0.002).Despite no skin conductance response group differences during extinction recall, brain activation patterns between anxious and healthy individuals differed. These findings encourage future studies to examine the conditions longitudinally and in the context of treatment trials to improve and guide therapeutics via advanced neurobiological understanding of each disorder.

Dataset Information

BDNFval66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall.

Publications

BDNFval66met affects neural activation pattern during fear conditioning and 24 h delayed fear recall.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets