ArticleJournal of pain research2026
Peripheral Sympathetic Sprouting Drives Neuropathic Pain via Spinal Microglial P2Y12 Activation in a Rat Spinal Nerve Ligation Model.
Article in Journal of pain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sympathetically maintained pain (SMP) is heterogeneous, and sympathetic sprouting is not universal across neuropathic pain states. In the rat spinal nerve ligation (SNL) model, peripheral sympathetic-sensory coupling may amplify spinal neuroinflammation. We examined whether peripheral sympathetic drive and spinal microglial P2Y12 signaling operate as parallel pathways or as a coupled peripheral-to-central axis. Methods: Male Sprague-Dawley rats were assigned to Sham, SNL, SNL + 6-OHDA, SNL + intrathecal ticagrelor, ticagrelor-only, or SNL + combined 6-OHDA/ticagrelor groups. Mechanical allodynia, microglial morphology, P2Y12/Iba-1 expression, p38 MAPK phosphorylation, and spinal cytokines were assessed by von Frey testing, immunofluorescence, Western blotting, and ELISA. A pharmacological occlusion paradigm tested pathway additivity. Results: SNL produced marked ipsilateral mechanical allodynia. On postoperative day 7, 6-OHDA increased paw withdrawal threshold from 3.56 to 8.43 g (Hedges' g=2.56, 95% CI 1.03 to 4.10) and reduced SNL-induced spinal P2Y12, Iba-1, p-p38/t-p38, and TNF-α/IL-1β/IL-6 increases. Intrathecal ticagrelor similarly attenuated allodynia (4.64 to 7.84 g; Hedges' g=1.45, 95% CI 0.23 to 2.67). In the occlusion experiment, AUCs were higher in SNL + 6-OHDA (50.11±4.94 g.day), SNL + ticagrelor (55.83±10.79 g.day), and combined treatment (52.85±9.28 g.day) than in SNL (25.09±8.78 g.day), with no additional benefit of combination therapy. Conclusion: These findings support a functional peripheral-to-central neuroimmune axis in which peripheral sympathetic activity amplifies spinal microglial P2Y12-p38 signaling in the SNL model. Purinergic interfaces may represent potential SMP targets, but clinical translation requires further validation.
Indexed as
Identifiers
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.