ArticleJournal of pain research2020
Early Blockade of EphA4 Pathway Reduces Trigeminal Neuropathic Pain.
Article in Journal of pain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Botulinum toxin type E alleviates trigeminal neuropathic pain via modulation of the HIF-1α-NLRP3 pathway.Frontiers in toxicology · 2026Article
- Rat adipose-derived mesenchymal stem cell-derived exosomes loaded with miR-375 promote neurite outgrowth and peripheral nerve regeneration via activation of Akt by targeting EPHA4.Regenerative therapy · 2025Article
- Can Botulinum Toxin Type E Serve as a Novel Therapeutic Target for Managing Chronic Orofacial Pain?Toxins · 2025Article
- Blockade of Piezo2 Pathway Attenuates Inflammatory and Neuropathic Pain in the Orofacial Area.Pain research & management · 2024Article
- Role of spinal astrocytes through the perisynaptic astrocytic process in pathological pain.Molecular brain · 2023Review
- Differential Regulation of Intracisternally Injected Angiotensin II-Induced Mechanical Allodynia and Thermal Hyperalgesia in Rats.Biomedicines · 2023Article
- Axon Guidance Molecules and Pain.Cells · 2022Review
- Potential Molecular Targets for Treating Neuropathic Orofacial Pain Based on Current Findings in Animal Models.International journal of molecular sciences · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the Eph receptor plays an important role in the development of neuropathic pain following nerve injury, there has been no evidence of the participation of the ephrin A4 receptor (EphA4) in the development of trigeminal neuropathic pain. The present study investigated the role of EphA4 in central nociceptive processing in rats with inferior alveolar nerve injury. MATERIALS AND
methodsMale Sprague-Dawley rats were used in all our experiments. A rat model for trigeminal neuropathic pain was produced using malpositioned dental implants. The left mandibular second molar was extracted under anesthesia, followed by the placement of a miniature dental implant to injure the inferior alveolar nerve.
resultsOur current findings show that nerve injury induced by malpositioned dental implants evokes significant mechanical allodynia and up-regulation of EphA4 expression in the ipsilateral trigeminal subnucleus caudalis. Although daily treatment with EphA4-Fc, an EphA4 antagonist, did not produce prolonged anti-allodynic effects after the chronic neuropathic pain had been already established, an early treatment protocol with repeated EphA4-Fc administration significantly attenuated mechanical allodynia before initiation of chronic neuropathic pain. Finally, we confirmed the participation of the central EphA4 pathway in the development of trigeminal neuropathic pain by reducing EphA4 expression using EphA4 siRNA. This suppression of EphA4 produced significantly prolonged anti-allodynic effects.
conclusionThese results suggest that early blockade of central EphA4 signaling provides a new therapeutic target for the treatment of trigeminal neuropathic pain.
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