A role of chemokine CCL2 and CX3CL1 in the induction of orofacial mechanical hyperalgesia
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| Year of publication | 2021 |
| Type | Conference abstract |
| MU Faculty or unit | |
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| Description | Trigeminal neuropathic pain caused by damage to the trigeminal nerve is very intense and extremely stressful compared to other types of neuropathic pain. Released chemokines during trigeminal nerve injury contribute to induction and maintenance of orofacial neuropathic pain. The role of CCL2 and CX3CL1 was investigated in the induction of orofacial mechanical hyperalgesia in the trigeminal ganglion (TG) following unilateral ligature of the infraorbital nerve (IONL). The IONL- and sham-operated rats survived for 1, 3, 7 and 14 days (n=6 each group). Von Frey monofilaments was used for measurement of mechanical hyperalgesia. The rats were perfused with Zamboni solution and TG was dissected. Longitudinal cryostat sections (12µm) were immunostained under the same conditions to explore immunodetection of CCL2 and CX3CL1. Mechanical hyperalgesia occurred and persisted bilaterally until postoperative day 7 (POD7) in sham-operated rats and POD14 in the rats after the unilateral IONL. The immunodetection of CCL2 and CX3CL1 was found bilaterally in both V1/2 and V3 compartments of TG after unilateral IONL. This indicated a spread of inflammatory conditions throughout the TG compartments with activation of both injured and noninjured neurons. The CCL2 immunofluorescence increased while CX3CL1 decreased from POD1 to POD 14. Elevation of CCL2 was associated with the development of mechanical hypersensitivity in bilateral vibrissal pads. Chemokines CCL2 and CX3CL1 play probably a different role in sensitization of the first order neurons of the trigeminal pathway and, therefore, may become a therapeutic target for the treatment of trigeminal hyperalgesia. |
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