Research Article

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 2

(a) EAE animals: thermal testing for tail. This figure illustrates withdrawal latencies of thermal sensory testing in the tails from EAE animals at different times in the disease progression. Data are aligned on the “x axis” to day of onset of neurological disability, where day 0 (=EAE9) is the first day of disease onset (where all EAE animals displayed some form of neurological disability). For example, day 5 is a representative of 5 days following disease onset which equates to EAE14. However, days −4 to −1 (baseline) represent the days prior to the onset of neurological disability that equate to EAE5, EAE6, EAE7, and EAE8 days post-induction. All values were normalized to average baseline withdrawal latencies and displayed as means standard error of the mean (SEM). Tail withdrawal latency was significantly elevated at day 0 (day of disease onset = EAE9) compared to the average baseline withdrawal latency, indicative of thermal hypoalgesia in the EAE animals ( using one sample t-test). Following this peak at EAE9, the thermal latency for tail declined and remained stable over the time period of EAE10 to EAE14 days following induction. Withdrawal latencies at baseline were not statistically significantly different from these depicted for days 1, 2, 3, 4 and 5 after disease onset. Errors bars represent SEM. (b, c) EAE animals: thermal testing for hindlimbs and forelimbs. (b, c) illustrate withdrawal latencies of thermal sensory testing in the hindlimb and forelimb of EAE animals at different times in the disease progression. Data are aligned on the “x axis” to day of onset of neurological disability, where day 0 (=EAE9) is the first day of disease onset (where all EAE animals displayed some form of neurological disability). For example, day 5 is a representative of 5 days following disease onset which equates to EAE14. However, days −4 to −1 (baseline) represent the days prior to the onset of neurological disability that equate to EAE5, EAE6, EAE7, and EAE8 days following induction. All values were normalized to average baseline withdrawal latencies and displayed as means standard error of the mean (SEM). (b) A statistically significant increase ( ) of the withdrawal latency characteristic of thermal hypoalgesia was observed in the left hind limb at day 4 following the onset of the disease compared to that of average baseline withdrawal latency (days −1 to −4 inclusive) and to day 0 (onset of neurological disability). (c) Similarly, a statistically significant increase ( ) of the withdrawal latency characteristic of thermal hypoalgesia was observed in the right and left forelimbs at day 4 following the onset of the disease compared to average baseline withdrawal latency (days −1 to −4 inclusive); day 0 (onset of neurological disability) and days 1 and 2 after disease onset. Errors bars represent standard error of the mean SEM.
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