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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Pain. 2013 Nov 21;155(3):476–484. doi: 10.1016/j.pain.2013.11.007

Figure 1.

Figure 1

Systemic artemin promotes recovery of tactile and thermal hypersensitivity following peripheral nerve crush, axotomy or ligation. The rats received subcutaneous injections of 1mg/kg artemin on a schedule of MWF (arrows) or vehicle for two weeks. Artemin treated rats showed partial reversal of L5 nerve-crush induced tactile (A) and thermal hypersensitivity (B) by the end of the first week of treatment. Tactile hypersensitivity returned by the first week following termination of artemin treatment, followed by a gradual recovery of sensory thresholds to pre-injury values across the remaining test period (A). Thermal hypersensitivity returned by the first week following termination of artemin treatment, followed by a gradual return of sensory thresholds towards pre-injury values in both vehicle and artemin treated rats (B). Artemin treated rats showed partial reversal of L5 axotomy-induced tactile (C) and thermal (D) hypersensitivity by the end of the first week of treatment. Tactile and thermal hypersensitivity returned following termination of artemin treatment and persisted for the remainder of the testing period. Artemin treated rats showed partial reversal of L5 ligation-induced tactile (E) and thermal (F) hypersensitivity by the end of the first week of treatment. Tactile and thermal hypersensitivity returned following termination of artemin treatment and persisted for the remainder of the testing period. sham-operated rats did not demonstrate any significant changes in tactile (G) or thermal (H) sensory thresholds either with artemin or vehicle treatment. Error bars indicate mean ± SEM. n = 8 per group. Asterisks indicate significance (P < 0.05) between artemin and vehicle treated groups.