TRPA1 activation mediates nociception behaviors in a mouse model of relapsing-remitting experimental autoimmune encephalomyelitis
| Autor: | Juliano Ferreira, Maria Fernanda Pessano Fialho, Gabriela Trevisan, Diéssica Padilha Dalenogare, Sabrina Qader Kudsi, Camila dos Santos Ritter, Débora Denardin Lückemeyer, Marcella de Amorim Ferreira, Maria Carolina Theisen, Sara Marchesan Oliveira, Caren Tatiane de David Antoniazzi, Diulle Spat Peres |
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| Rok vydání: | 2020 |
| Předmět: |
Nociception
0301 basic medicine Encephalomyelitis Autoimmune Experimental Pharmacology Mice 03 medical and health sciences chemistry.chemical_compound Transient receptor potential channel 0302 clinical medicine Developmental Neuroscience medicine Animals TRPA1 Cation Channel NADPH oxidase biology business.industry Multiple sclerosis Experimental autoimmune encephalomyelitis medicine.disease Mice Inbred C57BL 030104 developmental biology Allodynia Neurology chemistry Hyperalgesia Neuropathic pain Apocynin biology.protein Neuralgia Female medicine.symptom business psychological phenomena and processes 030217 neurology & neurosurgery |
| Zdroj: | Experimental Neurology. 328:113241 |
| ISSN: | 0014-4886 |
| Popis: | Central neuropathic pain is the main symptom caused by spinal cord lesion in relapsing-remitting multiple sclerosis (RRMS), but its management is still not effective. The transient receptor potential ankyrin 1 (TRPA1) is a pain detecting ion channel involved in neuropathic pain development. Thus, the aim of our study was to evaluate the role of TRPA1 in central neuropathic nociception induced by relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) mouse model. In this model, we observed the development of similar clinical conditions of RRMS in C57BL/6 female mice through RR-EAE using MOG35-55 antigen and Quil A adjuvant. At the thirty-fifth day post-induction, C57BL/6 female mice demonstrated alteration in the RR-EAE score without motor impairment, mechanical and cold allodynia. Also, significative changes in demyelinating (Mog and olig-1) and neuroinflammatory (Iba1, Gfap and Tnfa) markers were observed, but this model did not alter Trpa1 RNA expression levels in the spinal cord. The hydrogen peroxide and 4-hydroxynonenal levels (TRPA1 agonists) were increased in RR-EAE induced mice, as well as the NADPH oxidase activity. The intragastric treatment of RR-EAE induced mice with TRPA1 antagonists (HC-030031 and A-967079) and antioxidant (α-lipoic acid and apocynin) caused an antiallodynic effect. Moreover, the intrathecal administration of TRPA1 antisense oligonucleotide, HC-030031, α-lipoic acid, and apocynin transiently attenuated mechanical and cold allodynia. Thus, TRPA1 plays a key role in the induction of neuropathic pain in this model of RR-EAE and can be a possible target for investigating the development of pain in RRMS patients. |
| Databáze: | OpenAIRE |
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