@entity2951 treatment inhibits XXXX and @entity1931 induced by chronic constriction injury to the sciatic nerve in @entity35 .

@entity10133 @entity1931 @entity2951 @entity2331 @entity35 @entity8638 @entity13624
@entity8638 ( @entity8638 ) to the @entity35 sciatic nerve results in @entity2331 in the affected hind limb. One possible mechanism for this @entity2331 is @entity13624 , in which neuropeptides, represented by substance @entity10133 ), are involved. We attempted to determine whether @entity2951 treatment, which can deplete SP from nerve terminals, is effective in inhibiting @entity2331 induced by @entity8638 . @entity2951 (total dose, 125 mg/kg) or the vehicle alone was given intraperitoneally to adult @entity35 2 days before (Experiment 1) and 7 days after (Experiment 2) @entity8638 surgery. Paw withdrawal latency (PWL) was measured prior to and every week for 5 weeks after surgery. Bone mineral density (BMD) and the number of osteoclasts in tibial bones were determined 5 weeks after surgery. In @entity35 treated with the vehicle, BMD on the @entity8638 side was decreased significantly, while the number of osteoclasts was significantly increased in both experiments. @entity2951 treatment either before or 1 week after surgery inhibited the decreases in BMD as well as the increase in the number of osteoclasts on the @entity8638 side. PWL for the @entity8638 side in the vehicle group was significantly shorter than for the sham side in both experiments. However, @entity2951 treatment before surgery resolved @entity1931 in Experiment 1, while in Experiment 2, even though @entity1931 developed on the @entity8638 side, it was resolved by @entity2951 treatment. The results of the present study show that @entity2951 inhibits the development of @entity2331 as well as @entity1931 induced by @entity8638 . They also support our hypothesis that neurogenic SP release is involved in the pathogenesis of bony changes induced by @entity8638 .
