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- Title
Amygdala and nucleus accumbens involvement in appetitive extinction.
- Authors
Kruse, Onno; Klein, Sanja; Tapia León, Isabell; Stark, Rudolf; Klucken, Tim
- Abstract
Extinction of appetitive conditioning is regarded as an important model for the treatment of psychiatric disorders like addiction. However, very few studies have investigated its neural correlates. Therefore, we investigated neural correlates of appetitive extinction in a large human sample including all genders (N = 76, 40 females) to replicate and extend results from a previous study. During differential appetitive conditioning, one stimulus (CS+) was paired with the chance to win a monetary reward, whereas another stimulus (CS−) was not. During appetitive extinction on the next day, neither the CS+ nor the CS− were reinforced. After successful acquisition of appetitive conditioning, the extinction phase elicited significant reductions of valence and arousal ratings toward the CS+ and a significant reduction in skin conductance responses to the CS+ from early to late extinction. On a neural level, early extinction showed significant differential (CS+ − CS−) activation in dACC and hippocampus, whereas involvement of the vACC and caudate nucleus did not replicate. The differential activation of amygdala and nucleus accumbens during late extinction was replicated, with the amygdala displaying significantly higher differential activation during the late phase of extinction as compared to the early phase of extinction. We show discernible signals for reward learning and extinction in subregions of amygdala and nucleus accumbens after extinction learning. This successful replication underlines the role of nucleus accumbens and amygdala in neural models of appetitive extinction in humans that was previously only based on animal findings.
- Subjects
NUCLEUS accumbens; AMYGDALOID body; BIOLOGICAL extinction; GALVANIC skin response; CAUDATE nucleus
- Publication
Human Brain Mapping, 2020, Vol 41, Issue 7, p1833
- ISSN
1065-9471
- Publication type
Article
- DOI
10.1002/hbm.24915