Change of vanilloid receptor 1 following neuromodulation in rats with spinal cord injury.

BACKGROUND

Neuromodulation has been used to treat voiding dysfunction caused by spinal cord injury (SCI). However, the underlying mechanism of this technique is not well understood. Recently, vanilloid receptor 1 (VR1) has been recognized as a capsaicin receptor and an agent for noxious stimuli. The purposes of this study were to evaluate whether development of bladder hyperreflexia after SCI involves VR1 upregulation and whether VR1 is involved in the process of neuromodulation.

MATERIALS AND

METHODS

Sprague-Dawley rats (n = 20) were divided into five groups: sham control (n = 4); 3 days after SCI (n = 4); 7 days after SCI (n = 4); 14 days after SCI (n = 4), and 14 days after SCI with neurostimulation (n = 4). Bilateral electrode wires were implanted into S1 dorsal foramina and electrical stimulation was performed 8 h/day for 2 weeks. Spinal segments of L6, S1, and dorsal root ganglia were removed and cut into sections. The intensity of VR1 staining was evaluated by image analysis.

RESULTS

VR1-positive staining was confined to the superficial dorsal horn of the spinal cord. The staining was weak in the sham group (1/luminosity: 0.0050 +/- 0.0006), but the staining intensity was significantly increased in three SCI groups (3 days, 7 days, and 14 days) when compared with that in the sham group (P < 0.05). After neuromodulation, the staining intensity was reduced.

CONCLUSIONS

VR1 expression in the spinal cord is up-regulated after SCI. Sacral nerve root stimulation can down-regulate the VR1 expression.