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<p>In our prior study involving a transdiagnostic sample of individuals with anhedonia, we showed that an 8-week administration of a selective κ-opioid receptor (KOR) antagonist enhanced fMRI ventral striatal activation during reward anticipation in the Monetary Incentive Delay task as compared to a placebo. However, individual differences in brain architecture may limit the translation of this finding to the context of precision medicine. Here, we adopted an individual-specific approach to elucidate the effects of selective KOR antagonism on cortical-subcortical reward circuits in individuals with anhedonia. Sixty-four participants with anhedonia (30 KOR Antagonist, 34 Placebo) who completed both pre- and post- treatment MRI scans in the FAST-MAS study were included in this analysis. Using an individualized-brain-systems-functional-brain-mapping approach, functional networks were mapped at the individual level, and individual-specific cortical patches and subcortical-cortical clusters were obtained. Statistical analyses were conducted to examine the pre- and post-treatment changes in patch and cluster sizes, as well as their relationships with clinical-cognitive measures. ROI analyses revealed a significant patch size decrease in the right medial posterior prefrontal cortex within the frontoparietal control network, and significant size increases in three right subcortical clusters – pallidum, amygdala, and thalamus – within the orbitofrontal-limbic network, following KOR antagonist treatment. In short,&#xa0;we applied recently developed computational neuroimaging approaches to examine changes in the individualized brain systems of FAST-MAS participants before and after eight weeks of KOR antagonist treatment for anhedonia. Our results revealed alterations in functional cortical patch and subcortical-cortical cluster sizes in anhedonia-related brain regions following KOR antagonist treatment.</p>

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Selective KOR antagonist alters functional patch sizes in individualized brain system: results from the Fast-fail Trial in Mood and Anxiety Spectrum Disorders (FAST-MAS)

  • 期刊论文

  • 发表日期：

    2025年5月13日

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  • Hoki Fung,
  • Ruby M. Potash,
  • Andrew Krystal,
  • Diego A. Pizzagalli,
  • Matthew D. Sacchet

摘要

In our prior study involving a transdiagnostic sample of individuals with anhedonia, we showed that an 8-week administration of a selective κ-opioid receptor (KOR) antagonist enhanced fMRI ventral striatal activation during reward anticipation in the Monetary Incentive Delay task as compared to a placebo. However, individual differences in brain architecture may limit the translation of this finding to the context of precision medicine. Here, we adopted an individual-specific approach to elucidate the effects of selective KOR antagonism on cortical-subcortical reward circuits in individuals with anhedonia. Sixty-four participants with anhedonia (30 KOR Antagonist, 34 Placebo) who completed both pre- and post- treatment MRI scans in the FAST-MAS study were included in this analysis. Using an individualized-brain-systems-functional-brain-mapping approach, functional networks were mapped at the individual level, and individual-specific cortical patches and subcortical-cortical clusters were obtained. Statistical analyses were conducted to examine the pre- and post-treatment changes in patch and cluster sizes, as well as their relationships with clinical-cognitive measures. ROI analyses revealed a significant patch size decrease in the right medial posterior prefrontal cortex within the frontoparietal control network, and significant size increases in three right subcortical clusters – pallidum, amygdala, and thalamus – within the orbitofrontal-limbic network, following KOR antagonist treatment. In short, we applied recently developed computational neuroimaging approaches to examine changes in the individualized brain systems of FAST-MAS participants before and after eight weeks of KOR antagonist treatment for anhedonia. Our results revealed alterations in functional cortical patch and subcortical-cortical cluster sizes in anhedonia-related brain regions following KOR antagonist treatment.