Abstract
Exposure therapy for anxiety disorders relies on the principle of confronting a patient with the triggers of his fears, allowing him to make the unexpected safety experience that his fears are unfounded and resulting in the extinction of fear responses. In the laboratory, fear extinction is modeled by repeatedly presenting a fear-conditioned stimulus (CS) in the absence of the aversive unconditioned stimulus (UCS) to which it had previously been associated. Classical associative learning theory considers extinction to be driven by an aversive prediction error signal that expresses the expectation violation when not receiving an expected UCS and establishes a prediction of CS non-occurrence. Insufficiencies of this account in explaining various extinction-related phenomena could be resolved by assuming that extinction is an opponent appetitive-like learning process that would be mediated by the mesostriatal dopamine (DA) system. In accordance with this idea, we find that a functional polymorphism in the DA transporter gene, DAT1, which is predominantly expressed in the striatum, significantly affects extinction learning rates. Carriers of the 9-repeat (9R) allele, thought to confer enhanced phasic DA release, had higher learning rates. Further, functional magnetic resonance imaging revealed stronger hemodynamic appetitive prediction error signals in the ventral striatum in 9R carriers. Our results provide a first hint that extinction learning might indeed be conceptualized as an appetitive-like learning process and suggest DA as a new candidate neurotransmitter for human fear extinction. They open up perspectives for neurobiological therapy augmentation.
Highlights
Classical associative learning theory explains fear conditioning by an aversive prediction error signal dav generated when an initially non-predictive conditioned stimulus (CS) is unexpectedly followed by an unconditioned stimulus (UCS)
Classical associative learning theory considers extinction to be driven by an aversive prediction error signal that expresses the expectation violation when not receiving an expected UCS and establishes a prediction of CS non-occurrence. Insufficiencies of this account in explaining various extinction-related phenomena could be resolved by assuming that extinction is an opponent appetitive-like learning process that would be mediated by the mesostriatal dopamine (DA) system. In accordance with this idea, we find that a functional polymorphism in the DA transporter gene, DAT1, which is predominantly expressed in the striatum, significantly affects extinction learning rates
In the RW model of associative learning, the prediction error dav is weighted by a constant a, the learning rate, that determines how much a deviation from prediction at trial t is taken into account when formulating the prediction for the trial t þ 1
Summary
Classical associative learning theory explains fear conditioning by an aversive prediction error signal dav generated when an initially non-predictive conditioned stimulus (CS) is unexpectedly followed by an unconditioned stimulus (UCS) This establishes a UCS prediction, or aversive value Vav, for the CS that grows over successive pairings.[1,2] If at some point the UCS is unexpectedly omitted, this generates a negative (oppositely signed) aversive prediction error that will reduce Vav. This establishes a UCS prediction, or aversive value Vav, for the CS that grows over successive pairings.[1,2] If at some point the UCS is unexpectedly omitted, this generates a negative (oppositely signed) aversive prediction error that will reduce Vav The latter mechanism is thought to underlie the extinction of conditioned fear responses by repeated unpaired CS presentations.[1] It is the theoretical basis of exposure therapy where a patient is repeatedly confronted with the trigger of his fears (the CS, for example, in an agoraphobic, an open space) and makes the experience that the predicted outcome (the UCS) is absent or less disastrous than expected (for example, he does not collapse).[3]. A frequent finding is that conditioned fear responses can return after successful extinction, indicating that the CS–UCS association (Vav) is not unlearned or erased during extinction but rather complemented by a competing inhibitory CS–noUCS association that may, or may not, dominate the CS–UCS association at future CS presentations.[4,5,6] there is compelling evidence for a partial segregation in the neural systems subserving conditioning and extinction.[7,8,9,10,11,12] The above simple account of extinction, as being solely mediated by the same learning system that mediates conditioning, cannot accommodate these observations
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
