Journal
SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
Volume 10, Issue 12, Pages 1730-1737Publisher
OXFORD UNIV PRESS
DOI: 10.1093/scan/nsv061
Keywords
neuropeptide S; NPSR1; emotional working memory; anxiety; fNIRS
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Funding
- German Research Foundation [SFB-TRR 58, B06, C02, C06, Z02]
- DFG
- Lander funds [RTG 1256/2]
- BMBF [01EO1004]
- LEAD graduate school, a project of the Excellence Initiative of the German federal and state governments [GSC1028]
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The neuropeptide S (NPS) and its receptor NPSR have captured attention in the pathogenesis of anxiety disorders. Here, a functional polymorphism in the NPSR1 gene has been linked to deviant cortico-limbic interactions in response to negative stimuli. While healthy T allele carriers exhibited increased amygdala and prefrontal cortex activity, panic disorder patients carrying the T risk allele displayed hypofrontality possibly reflecting insufficient prefrontal inhibition of limbic reactivity. In order to study multi-level effects of genotype and anxiety, prefrontal cortex activity during an emotional n-back task was measured in 66 volunteers genotyped for the NPSR1 rs324981 A/T variant (AA homozygotes vs. T allele carriers) by means of functional near-infrared spectroscopy. For a high working memory load (3-back), T allele carriers showed a signal increase to negative pictures in the dorsolateral and medial prefrontal cortex while AA homozygotes displayed a signal decrease. Since groups did not differ on skin conductance level and behavioral parameters, this effect in the risk group in line with results from fMRI studies is speculated to represent an adaptive mechanism to compensate for presumably increased subcortical activity driven by an overactive NPS system. However, anxiety sensitivity correlated negatively with prefrontal activity in T allele carriers possibly suggesting a decompensation of the adaptive compensatory upregulation.
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