ArticlePain2015
Differential contributions of A- and C-nociceptors to primary and secondary inflammatory hypersensitivity in the rat.
Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Pulsed 830-nm Laser Irradiation Modulates Aδ- and C-Fiber-Mediated Pain Thresholds in Healthy Adults: A Randomized, Sham-Controlled Trial.Lasers in surgery and medicine · 2026Trial
- Modulation of TNF-α, IL-1β and myeloperoxidase contributes to the anti-inflammatory and analgesic effects of Paullinia pinnata Linn (Sapindaceae) extracts in complete Freund's adjuvant-induced mono-arthritis in rats.Journal of ethnopharmacology · 2026Article
- Acid-sensing ion channels and their role in controlling pain in the post-operative stage.International journal of physiology, pathophysiology and pharmacology · 2026Review
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- Assessing signs of central sensitization: A critical review of physiological measures in experimentally induced secondary hyperalgesia.European journal of pain (London, England) · 2025Review
- Repetitive Transcranial Magnetic Stimulation: Is it an Effective Treatment for Cancer Pain?Pain and therapy · 2025Review
- Role of TMEM100 in mechanically insensitive nociceptor un-silencing.Nature communications · 2023Article
- Peripheral CCL2 induces inflammatory pain via regulation ofFrontiers in molecular neuroscience · 2023Article
- Noxious radiant heat evokes bi-component nociceptive withdrawal reflexes in spinal cord injured humans-A clinical tool to study neuroplastic changes of spinal neural circuits.Frontiers in human neuroscience · 2023Article
- Effects of buprenorphine on acute pain and inflammation in the adjuvant-induced monoarthritis rat model.Heliyon · 2022Article
- When Differential Descending Control of Speed Matters: Descending Modulation of A- versus C-Fiber Evoked Spinal Nociception.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Cutaneous pain in disorders affecting peripheral nerves.Neuroscience letters · 2021Review
- Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain-Narrative Review.Pharmaceutics · 2021Review
- Peripheral Mechanisms of Neuropathic Pain-the Role of Neuronal and Non-Neuronal Interactions and Their Implications for Topical Treatment of Neuropathic Pain.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Segmental Chiropractic Spinal Manipulation Does not Reduce Pain Amplification and the Associated Pain-Related Brain Activity in a Capsaicin-Heat Pain Model.Frontiers in pain research (Lausanne, Switzerland) · 2021Article
- Doxepin prevents the Expression and Development of Paclitaxel-Induced Neuropathic Pain.Advanced biomedical research · 2021Article
- A New Apparatus for Recording Evoked Responses to Painful and Non-painful Sensory Stimulation in Freely Moving Mice.Frontiers in neuroscience · 2021Article
- Aqueous and methanol extracts of Paullinia pinnata L. (Sapindaceae) improve inflammation, pain and histological features in CFA-induced mono-arthritis: Evidence from in vivo and in vitro studies.Journal of ethnopharmacology · 2019Article
- Contact Heat Evoked Potentials Are Responsive to Peripheral Sensitization: Requisite Stimulation Parameters.Frontiers in human neuroscience · 2019Article
- VEGFR2 promotes central endothelial activation and the spread of pain in inflammatory arthritis.Brain, behavior, and immunity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Primary hyperalgesia is characterized by increased responsiveness to both heat and mechanical stimulation in the area of injury. By contrast, secondary hyperalgesia is generally associated with increased responses to mechanical but not heat stimuli. We tested the hypothesis that sensitization in secondary hyperalgesia is dependent on the class of peripheral nociceptor (C- or A-nociceptor) rather than the modality of stimulation (mechanical vs heat). A- and C-nociceptors were selectively activated using contact heat ramps applied to the hind paw dorsum in animals with hind paw inflammation (primary hyperalgesia) and knee inflammatory arthritis (secondary hyperalgesia). Sensitization to A- and C-nociceptor activation in primary and secondary hyperalgesia was assessed by reflex withdrawal thresholds and by Fos immunocytochemistry in the dorsal horn of the spinal cord, as an index of neuronal activation. In primary hyperalgesia, only C-nociceptor-evoked withdrawal reflexes were sensitized. This was associated with increased spinal lamina I neuronal activation to both A- and C-nociceptor activation. Fos-like immunoreactivity (FLI) was unchanged in other dorsal horn laminae. In secondary hyperalgesia, only A-nociceptor-evoked withdrawal reflexes were sensitized, and FLI was increased in both superficial and deep dorsal laminae. Neurons in the superficial dorsal horn receive and process nociceptor inputs from the area of primary hyperalgesia, resulting in functional sensitization to C-nociceptive inputs. In inflammatory arthritis, secondary hyperalgesia is evoked by A-nociceptor thermal stimulation, suggesting that secondary hyperalgesia is A-nociceptor, rather than stimulus modality (mechanical vs thermal), dependent. Fos-like immunoreactivity evoked by A-nociceptor stimulation in secondary hyperalgesia suggests that the sensitization is underpinned by spinal neuronal sensitization in laminae I and IV/V.
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What OpenQuestion holds
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.