The effect of low power GaAlAs laser stimulation on anti-nociception and spinal neuronal activity related to pain sensation in the polyarthritis of rats

다발성 관절염 실험동물 모델에서 저출력 GaAlAs 레이저 자극의 진통효능 및 통증관련 척수내 신경세포의 활성변화에 관한 연구

The experiments were designated to evaluate the anti-nociceptive effect of low power laser stimulation on acupoint or non-acupoint using arthrogenic solution induced poly arthritis animal model. Evaluation of potential antinociceptive effect of low power laser on arthritis has employed measurements of the foot bending test, the development of either thermal or mechanical hyperalgesia following the arthritis induction. The analysis of thermal hyperalgesia includes Hargreaves's method. Randall-Sellitto test was utilized for evaluating mechanical hyperalgesia. In addition, the antinociceptive effect of low power laser stimulation on arthritis induced spinal Fos expression was analyzed using a computerized image analysis system. The results were summerized as follows: 1. In laser stimulation on acupoint treated animal, laser stimulation dramatically inhibited the development of pain in foot bending test as compared to those of non acupoint treated animal group and non treated animal group. 2. The threshold of thermal stimulation was significantly increased by low power laser stimulation on acupoint as compared to that of non treated control group. 3. Laser stimulation on acupoint dramatically attenuated the development of mechanical hyperalgesia as compared to that of non treated group. 4. Low power laser stimulation on acupoint significantly suppressed arthritis induced Fos expression in the lumbar spinal cord at 3 week post arthritis induction. In conclusion, the results of the present study demonstrated that low power laser stimulation on acupoint has potent anti-nociceptive effect on arthritis. Additional supporting data for an antinociceptive effect of laser stimulation was obtained using Fos immunohistochemical analysis on spinal cord section. Those data indicated that laser stimulation induced antinociception was mediated by suppression of spinal neuron activity in pain sensation.