ArticleNature communications2026
Cholecystokinin input from the anterior cingulate cortex to the lateral periaqueductal gray mediates nocebo pain behavior in mice.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Reduced MOV10 reveals novel functional cortical connections in an increased fear response.bioRxiv : the preprint server for biology · 2026Article
- Direct comparisons of neural activity during placebo analgesia and nocebo hyperalgesia between humans and rats.Communications biology · 2025Article
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Authors and funding
19 authors.
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Abstract
The nocebo effect, opposite of the better-known placebo effect, in which anticipation of harm worsens pain and other symptoms, is increasingly thought to be responsible for poor clinical outcomes. In humans, nocebo hyperalgesia (i.e., increased pain sensitivity) is blocked by proglumide, a cholecystokinin (CCK) receptor antagonist. Yet, the neural circuitry underlying nocebo hyperalgesia remains unidentified, largely due to a lack of appropriate animal models. Here, we developed distinct mouse models of CCK-dependent nocebo hyperalgesia in which the expectation of pain was elicited by contextual or social cues. We find that these nocebo paradigms share a neural circuit involving CCK release from neurons projecting from the anterior cingulate cortex to the lateral periaqueductal gray. This pathway could represent a promising target for therapeutic interventions in pain-related disorders.
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