Chemokine ligand 2/chemokine receptor 2 signaling in the trigeminal ganglia contributes to inflammatory hyperalgesia in rats
| Autor: | Masanori Nasu, Mamoru Takeda, Yoshihito Shimazu, Takuya Kanazawa, Masayuki Takahashi |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty CCR2 Chemokine medicine.drug_class Freund's Adjuvant Inflammation Stimulation Membrane Potentials 03 medical and health sciences Chemokine receptor Trigeminal ganglion 0302 clinical medicine Internal medicine medicine Animals Skin Neurons biology Chemistry General Neuroscience General Medicine Receptor antagonist Rats 030104 developmental biology Endocrinology Hyperalgesia Immunology biology.protein Receptors Chemokine medicine.symptom 030217 neurology & neurosurgery |
| Zdroj: | Neuroscience research. 128 |
| ISSN: | 1872-8111 |
| Popis: | This study investigated the functional significance of hyperalgesia in the CCL2/CCR2 signaling system in trigeminal ganglion (TG) neurons following inflammation. Inflammation was induced by injection of complete Freund's adjuvant (CFA) into the whisker pad of rats. The escape threshold from mechanical stimulation applied to the whisker pad 2days later was significantly lower in CFA-treated rats than in naive rats. Fluorogold (FG) labeling was used to identify the TG neurons innervating the whisker pad. FG-labeled TG neurons were immunoreactive for CCL2/CCR2. The mean number of CCL2/CCR2-immunoreactive small/medium-diameter TG neurons was significantly higher in inflamed rats than in naive rats. Using whole-cell patch-clamp experiments in small-diameter TG neurons, the threshold current of FG-labeled TG neurons in inflamed rats was significantly decreased compared to naive rats. The number of spike discharges during current injections by FG-labeled TG neurons in inflamed rats was significantly increased compared to naive rats. These characteristic effects were abolished by co-application of a CCL2 receptor antagonist. The present study provides evidence that CCL2 enhances the excitability of small-diameter TG neurons following facial skin inflammation via the upregulation of CCR2. These findings suggest that ganglionic CCL2/CCR2 signaling is a therapeutic target for the treatment of trigeminal inflammatory hyperalgesia. |
| Databáze: | OpenAIRE |
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