Up-regulation of calcitonin gene-related peptide in trigeminal ganglion following chronic exposure to paracetamol in a CSD migraine animal model |
| |
| Affiliation: | 1. Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand;2. Department of Physiology, Faculty of Dentistry, Chulalongkorn University, Bangkok 10330, Thailand;3. Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand;4. Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand;1. Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, Szigeti u. 12, H-7624 Pécs, Hungary;2. Research Division, Gedeon Richter Plc., H-1103 Budapest, Gyömrői út 19-21, Hungary;3. János Szentágothai Research Centre, University of Pécs, Ifjúság út 20, H-7624 Pécs, Hungary;4. Laboratory of Neuropharmacology, Pharmacological and Drug Safety Research, Gedeon Richter Plc., H-1103 Budapest, Gyömrői út 19-21, Hungary;5. Department of Anatomy, Faculty of Medicine, University of Pécs, Szigeti u. 12, H-7624 Pécs, Hungary;6. Neurology Department, University of Szeged, Faculty of Medicine, H-6725 Szeged, Semmelweis u. 6, Hungary;7. MTA-SZTE Neuroscience Research Group, H-6725 Szeged, Semmelweis u. 6, Hungary;8. MTA-PTE NAP B Chronic Pain Research Group, Faculty of Medicine, University of Pécs, Szigeti u. 12, H-7624 Pécs, Hungary;1. Department of Biomedical Sciences, University of Sassari, Viale San Pietro 43/b, 07100 Sassari, Italy;2. Department of Medical, Surgical and Experimental Sciences, University of Sassari, Italy;3. Institute of Bioimaging and Molecular Physiology, National Research Council, Genoa, Italy;4. Neurology Unit, A. Segni Hospital - ASL n. 1, Sassari, Italy;1. Cincinnati Children''s Hospital Medical Center, Cincinnati, OH, USA;2. Mayo Clinic, Rochester, MN, USA |
| |
| Abstract: | Previously, our group has demonstrated that chronic paracetamol (APAP) treatment induces alterations to the trigeminovascular nociceptive system in the cortical spreading depression (CSD) migraine animal model. The calcitonin gene related peptide (CGRP) is a key neuropeptide involved in the activation of the trigeminovascular nociceptive system. Therefore, this study examined the expression levels of CGRP in the trigeminal ganglion (TG) after chronic APAP exposure (0, 15, and 30 days) using a CSD model. Rats were divided into control, CSD only, APAP only and APAP treatment with CSD groups. A single injection (i.p.) of APAP (200 mg/kg body weight) was given to the 0-day APAP-treated groups, while the other APAP-treated groups received daily injections for 15 and 30 days. CSD was induced by the topical application of KCl to the parietal cortex. The protein expression of CGRP in the TG was evaluated by immunohistochemistry, and the CGRP mRNA level was investigated by real-time quantitative reverse transcription polymerase chain reaction. The results revealed that the induction of CSD significantly increased the level of CGRP protein but had no effect on CGRP mRNA level. Pretreatment with APAP 1 hour before CSD activation significantly reduced CGRP expression induced by CSD. In contrast, chronic treatment with APAP (15 and 30 days) significantly enhanced CGRP expression in both protein and mRNA levels when compared with the control groups. In combination with CSD, the expression of CGRP further increased in the animal with 30 day treatment. These findings indicate that chronic treatment with APAP induces an increase of CGRP expression in the TG. This alteration may be associated with the increased trigeminovascular nociception observed in our previous studies. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
