ArticleProceedings of the National Academy of Sciences of the United States of America2011
Tonic inhibition of chronic pain by neuropeptide Y.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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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.
The trial behind it
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Who cites it
80 citing papers in PubMed, 138 citations in OpenAlex.
- Moderated mediation for exercise maintenance in pain and posttraumatic stress disorder: A randomized trial.Health psychology : official journal of the Division of Health Psychology, American Psychological Association · 2020Trial
- Trial
- Hypothalamic prolactin receptorNature communications · 2026Article
- Spatial transcriptomics reveals organizational properties of mouse spinal cord and alterations in neuropathic pain.bioRxiv : the preprint server for biology · 2026Article
- What a pain in the back: etiology, diagnosis and future treatment directions for discogenic low back pain.Bone research · 2025Review
- The pharmacotherapeutic potential of neuropeptide Y for chronic pain.Journal of internal medicine · 2025Review
- Arrestin-biased allosteric modulator of neurotensin receptor 1 alleviates acute and chronic pain.Cell · 2025Article
- Neuropeptide Y neurons mediate opioid-induced itch by disinhibiting GRP-GRPR microcircuits in the spinal cord.Nature communications · 2025Article
- Mechanism-based nonopioid analgesic targets.The Journal of clinical investigation · 2025Review
- De novo expression of neuropeptide Y in sensory neurons does not contribute to peripheral neuropathic pain.The journal of pain · 2025Article
- Octanoic acid-rich diet alleviates breast cancer-induced bone pain via the acyl-ghrelin/NPY pathway.The Korean journal of pain · 2025Article
- Neuropeptide Y Y2 receptors in acute and chronic pain and itch.Neuropeptides · 2024Review
- Neuropeptide Y Y2 Receptors in Sensory Neurons Tonically Suppress Nociception and Itch but Facilitate Postsurgical and Neuropathic Pain Hypersensitivity.Anesthesiology · 2024Article
- Description of Novel Molecular Factors in Lumbar DRGs and Spinal Cord Factors Underlying Development of Neuropathic Pain Component in the Animal Model of Osteoarthritis.Molecular neurobiology · 2024Article
- Validity of Plasma Neuropeptide Y in Combination with Clinical Factors in Predicting Neuralgia Following Herpes Zoster.International journal of general medicine · 2024Article
- The plasticity of neuropeptide Y-Y1 receptor system onTheranostics · 2024Article
- Unloading-Induced Skeletal Interoception Alters Hypothalamic Signaling to Promote Bone Loss and Fat Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Contribution of µ Opioid Receptor-expressing Dorsal Horn Interneurons to Neuropathic Pain-like Behavior in Mice.Anesthesiology · 2023Article
- Endogenous μ-opioid-Neuropeptide Y Y1 receptor synergy silences chronic postoperative pain in mice.PNAS nexus · 2023Article
- Neuropeptide Y-expressing dorsal horn inhibitory interneurons gate spinal pain and itch signalling.eLife · 2023Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Dramatically up-regulated in the dorsal horn of the mammalian spinal cord following inflammation or nerve injury, neuropeptide Y (NPY) is poised to regulate the transmission of sensory signals. We found that doxycycline-induced conditional in vivo (Npy(tet/tet)) knockdown of NPY produced rapid, reversible, and repeatable increases in the intensity and duration of tactile and thermal hypersensitivity. Remarkably, when allowed to resolve for several weeks, behavioral hypersensitivity could be dramatically reinstated with NPY knockdown or intrathecal administration of Y1 or Y2 receptor antagonists. In addition, Y2 antagonism increased dorsal horn expression of Fos and phosphorylated form of extracellular signal-related kinase. Taken together, these data establish spinal NPY receptor systems as an endogenous braking mechanism that exerts a tonic, long-lasting, broad-spectrum inhibitory control of spinal nociceptive transmission, thus impeding the transition from acute to chronic pain. NPY and its receptors appear to be part of a mechanism whereby mammals naturally recover from the hyperalgesia associated with inflammation or nerve injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.