Elevated Expression of Fractalkine (CX3CL1) and Fractalkine Receptor (CX3CR1) in the Dorsal Root Ganglia and Spinal Cord in Experimental Autoimmune Encephalomyelitis: Implications in Multiple Sclerosis-Induced Neuropathic Pain

Figure 1

EAE animals Neurological Disability Clinical Score. All animals in the EAE groups were assessed for neurological disability according to a previously described global neurological disability assessment tool [26, 27] detailed in Table 1. Disability scores range from a mean clinical disability score of 0 (no disability) to 15 (maximum disability). The bell shaped distribution outlining peak neurological disability in response to EAE induction occurred at EAE12. Clinical neurological deficits appear at 6 days after antigenic induction. By EAE9 all animals started to display clinical signs of neurological disability (0.57 ± 0.45; mean ± SEM). Neurological disability progressively worsened upon daily assessment until EAE12 (peak disability; 6.42 ± 5.35) and then subsided by EAE15 (1.5 ± 1.41) as the animals entered the remission phase of disease induction, well characterized for this animal model. Errors bars represent SEM.