{
  "abstract": "Neuropathic pain results from damage to the nervous system and causes persistent changes in brain function that contribute to chronic pain. Understanding how these changes evolve over time is essential for identifying the mechanisms that sustain the disease. Here we show how brain-wide communication changes during the development and persistence of neuropathic pain in male mice using resting-state functional ultrasound imaging in awake and anesthetized animals. Pain onset is associated with transient increases in communication between brain regions involved in sensory, motivational, and emotional processing, whereas the persistent phase shows reduced communication within movement-related networks. Animals that undergo surgery without nerve injury also display lasting changes, revealing brain plasticity independent of neuropathic pain. Despite these network alterations, the overall organization of spontaneous brain activity remains stable. These findings reveal phase-dependent adaptations in brain circuits while preserving global resting-state brain dynamics.Pain is defined as an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage, and it often arises from a lesion or disease affecting the somatosensory system. Neuropathic pain represents a significant global health burden, affecting 7-10% of the population 1 . In this condition, lesioned sensory neurons transmit abnormal signals to the spinal cord and brain, producing characteristic symptoms, such as allodynia and hyperalgesia 2 . Over time, this altered signaling induces long-lasting central sensitization, leading to widespread electrophysiological, structural, and functional changes across various brain regions 3 .\n\nThese brain regions are often part of broader functional networks that serve multiple roles beyond pain perception, including emotional regulation and cognitive control. For instance, the cingulate cortex and the prefrontalamygdala axis are critically involved in both nociception and mood regulation. This overlap has led to the hypothesis that maladaptive plasticity in these hubs may underlie the high comorbidity of chronic pain with affective disorders, such as anxiety and depression 4 . While many studies have identified the brain regions activated during acute pain (often referred to as the 'pain matrix'), much less is known about how brain networks reorganize as pain becomes chronic. Pioneering work by Apkarian and colleagues revealed that functional connectivity (FC) between the nucleus accumbens (NAc) and other limbic and cortical structures could predict the transition to chronic pain in humans 5 , suggesting that network-level biomarkers may play a central role in pain chronification.\n\nResting-state functional connectivity has emerged as a promising approach for studying such brain-wide alterations. This method captures spontaneous fluctuations in neural activity, offering insights into the intrinsic organization of the brain and its longitudinal dynamics in both humans and animals 6-8 . In preclinical models, it allows researchers to track neural adaptations in controlled environments and over defined disease stages.\n\nAlthough most resting-state studies rely on static FC measures averaged over the entire recording period, spontaneous brain activity is increasingly recognized as dynamically organized into recurring functional.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 14,
  "authors": [
    {
      "name": "Silvia Cazzanelli"
    },
    {
      "name": "Samuel Le Meur-Diebolt"
    },
    {
      "name": "Jérome Baranger"
    },
    {
      "name": "Youenn Travert-Jouanneau"
    },
    {
      "name": "Luc Eglin"
    },
    {
      "name": "Ipek Yalcin"
    },
    {
      "name": "Adrien Bertolo"
    },
    {
      "name": "Alexandre Dizeux"
    },
    {
      "name": "Nathalie Ialy-Radio"
    },
    {
      "name": "Thomas Deffieux"
    },
    {
      "name": "Mickael Tanter"
    },
    {
      "name": "Bruno Felix Osmanski"
    },
    {
      "name": "Jeremy Ferrier"
    },
    {
      "name": "Sophie Pezet"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/8mr5mr7k3hazw.bib",
  "cited_by": 0,
  "doi": "10.1038/s42003-026-10922-5",
  "fulltext_url": null,
  "id": "8mr5mr7k3hazw",
  "issns": [
    "2399-3642"
  ],
  "landing_url": "https://hal.science/hal-05767276v1",
  "language": "en",
  "licence": "CC-BY-NC-ND-4.0",
  "licence_label": "CC BY-NC-ND 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.phys"
    ],
    [
      "hal",
      "0.sdv"
    ],
    [
      "openalex",
      "2805|Functional Brain Connectivity Studies"
    ]
  ],
  "openalex": "W7214080506",
  "pdf_url": "https://hal.science/hal-05767276/document",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-23",
  "publisher": "Nature Publishing Group",
  "ris": "https://research.draconitic.com/paper/8mr5mr7k3hazw.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:42Z",
      "native_id": "hal-05767276",
      "source": "hal",
      "url": "https://hal.science/hal-05767276v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "openalex:2805|Functional Brain Connectivity Studies",
      "subfield": "neuroscience"
    }
  ],
  "title": "Large-scale functional brain network organization is largely preserved in neuropathic pain despite selective circuit-level adaptations",
  "title_text": "Large-scale functional brain network organization is largely preserved in neuropathic pain despite selective circuit-level adaptations",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:42Z",
  "url": "https://research.draconitic.com/paper/8mr5mr7k3hazw",
  "venue": "Communications Biology",
  "versions": []
}