ArticleExperimental neurology2012
IB4-saporin attenuates acute and eliminates chronic muscle pain in the rat.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- PD-1/PD-L1 pathway relieves incision induced acute postoperative pain via inhibiting the neuroinflammation in dorsal root ganglion of rats.Scientific reports · 2025Article
- Resistance Training Before Hyperalgesia Induction Promotes Analgesic Effects Through Central and Peripheral Biomarker Modulation in an Experimental Fibromyalgia-like Model.Life (Basel, Switzerland) · 2025Article
- Saporin fromToxins · 2020Review
- Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments.Journal of dental research · 2020Review
- Non-Peptidergic Nociceptive Neurons Are Essential for Mechanical Inflammatory Hypersensitivity in Mice.Molecular neurobiology · 2019Article
- Review
- Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons.The Journal of clinical investigation · 2018Article
- Spontaneous and Bite-Evoked Muscle Pain Are Mediated by a Common Nociceptive Pathway With Differential Contribution by TRPV1.The journal of pain · 2017Article
- Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.Neuroscience letters · 2017Article
- Ambroxol for the treatment of fibromyalgia: science or fiction?Journal of pain research · 2017Article
- Role of Kv4.3 in Vibration-Induced Muscle Pain in the Rat.The journal of pain · 2016Article
- Article
- Whole-body Vibration at Thoracic Resonance Induces Sustained Pain and Widespread Cervical Neuroinflammation in the Rat.Clinical orthopaedics and related research · 2015Article
- Roles of ASIC3, TRPV1, and NaV1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia.Molecular pain · 2014Article
- Role for monocyte chemoattractant protein-1 in the induction of chronic muscle pain in the rat.Pain · 2014Article
- TREK2 expressed selectively in IB4-binding C-fiber nociceptors hyperpolarizes their membrane potentials and limits spontaneous pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Peripheral G protein-coupled inwardly rectifying potassium channels are involved in δ-opioid receptor-mediated anti-hyperalgesia in rat masseter muscle.European journal of pain (London, England) · 2014Article
- The fundamental unit of pain is the cell.Pain · 2013Review
- In vivo and in vitro comparison of female and male nociceptors.The journal of pain · 2012Article
- IB4(+) nociceptors mediate persistent muscle pain induced by GDNF.Journal of neurophysiology · 2012Article
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4 authors.
Funding
Abstract
The function of populations of nociceptors in muscle pain syndromes remain poorly understood. We compared the contribution of two major classes, isolectin B4-positive (IB4(+)) and IB4-negative (IB4(-)) nociceptors, in acute and chronic inflammatory and ergonomic muscle pain. Baseline mechanical nociceptive threshold was assessed in the gastrocnemius muscle of rats treated with IB4-saporin, which selectively destroys IB4(+) nociceptors. Rats were then submitted to models of acute inflammatory (intramuscular carrageenan)- or ergonomic intervention (eccentric exercise or vibration)-induced muscle pain, and each of the three models also evaluated for the transition from acute to chronic pain, manifest as prolongation of prostaglandin E2 (PGE(2))-induced hyperalgesia, after recovery from the hyperalgesia induced by acute inflammation or ergonomic interventions. IB4-saporin treatment did not affect baseline mechanical nociceptive threshold. However, compared to controls, IB4-saporin treated rats exhibited shorter duration mechanical hyperalgesia in all three models and attenuated peak hyperalgesia in the ergonomic pain models. And, IB4-saporin treatment completely prevented prolongation of PGE(2)-induced mechanical hyperalgesia. Thus, IB4(+) and IB4(-) neurons contribute to acute muscle hyperalgesia induced by diverse insults. However, only IB4+ nociceptors participate in the long term consequence of acute hyperalgesia.
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