eprintid: 21794 rev_number: 15 eprint_status: archive userid: 1589 dir: disk0/00/02/17/94 datestamp: 2016-08-22 12:13:07 lastmod: 2024-08-17 17:25:36 status_changed: 2016-08-22 12:13:07 type: article metadata_visibility: show creators_name: Lu, Jianning creators_name: Kurejova, Martina creators_name: Wirotanseng, Laura N. creators_name: Linker, Ralf A. creators_name: Kuner, Rohini creators_name: Tappe-Theodor, Anke title: Pain in experimental autoimmune encephalitis: a comparative study between different mouse models subjects: ddc-570 subjects: ddc-610 divisions: i-712000 divisions: i-718000 divisions: i-54600 abstract: Background: Pain can be one of the most severe symptoms associated with multiple sclerosis (MS) and develops with varying levels and time courses. MS-related pain is difficult to treat, since very little is known about the mechanisms underlying its development. Animal models of experimental autoimmune encephalomyelitis (EAE) mimic many aspects of MS and are well-suited to study underlying pathophysiological mechanisms. Yet, to date very little is known about the sensory abnormalities in different EAE models. We therefore aimed to thoroughly characterize pain behavior of the hindpaw in SJL and C57BL/6 mice immunized with PLP139-151 peptide or MOG35-55 peptide respectively. Moreover, we studied the activity of pain-related molecules and plasticity-related genes in the spinal cord and investigated functional changes in the peripheral nerves using electrophysiology. Methods: We analyzed thermal and mechanical sensitivity of the hindpaw in both EAE models during the whole disease course. Qualitative and quantitative immunohistochemical analysis of pain-related molecules and plasticity-related genes was performed on spinal cord sections at different timepoints during the disease course. Moreover, we investigated functional changes in the peripheral nerves using electrophysiology. Results: Mice in both EAE models developed thermal hyperalgesia during the chronic phase of the disease. However, whereas SJL mice developed marked mechanical allodynia over the chronic phase of the disease, C57BL/6 mice developed only minor mechanical allodynia over the onset and peak phase of the disease. Interestingly, the magnitude of glial changes in the spinal cord was stronger in SJL mice than in C57BL/6 mice and their time course matched the temporal profile of mechanical hypersensitivity. Conclusions: Diverse EAE models bearing genetic, clinical and histopathological heterogeneity, show different profiles of sensory and pathological changes and thereby enable studying the mechanistic basis and the diversity of changes in pain perception that are associated with distinct types of MS. date: 2012 publisher: BioMed Central id_scheme: DOI ppn_swb: 1659106575 own_urn: urn:nbn:de:bsz:16-heidok-217946 language: eng bibsort: LUJIANNINGPAININEXPE2012 full_text_status: public publication: Journal of Neuroinflammation volume: 9 number: 233 place_of_pub: London pagerange: 1-15 issn: 1742-2094 citation: Lu, Jianning ; Kurejova, Martina ; Wirotanseng, Laura N. ; Linker, Ralf A. ; Kuner, Rohini ; Tappe-Theodor, Anke (2012) Pain in experimental autoimmune encephalitis: a comparative study between different mouse models. Journal of Neuroinflammation, 9 (233). pp. 1-15. ISSN 1742-2094 document_url: https://archiv.ub.uni-heidelberg.de/volltextserver/21794/1/12974_2012_Article_788.pdf