Hyperalgesia in an animal model of multiple sclerosis.

摘要: Abstract Many individuals with multiple sclerosis (MS) experience clinically significant pain, yet the underlying neural mechanisms for MS pain are not understood. Experimental autoimmune encephalomyelitis (EAE) is a well-studied disease in rodents that mimics many clinical and pathological features of MS, including central nervous system inflammation demyelination. To determine whether EAE an appropriate model MS-related nociceptive responses both male female SJL mice were measured before after immunization myelin proteolipid protein peptide 139–151 (PLP139–151) complete Freund's adjuvant to induce ‘active’ EAE. if changes nociception due direct effects encephalitogenic T cells, following transfer activated, PLP139–151 specific cells ‘passive’ Both forepaw tail withdrawal latencies radiant heat stimulus measured. In active passive EAE, there was initial increase latency (hypoalgesia) peaked several days prior peak motor deficits during acute phase. During chronic phase, decreased significantly faster than control up 38 post-immunization. This hyperalgesia seen sexes models. Forepaw remained within 1–2 s baseline entire testing period, indicating hypoalgesia most pronounced affected body regions. These results suggest useful models pain.