摘要
目的:观察大鼠脑出血后脊髓运动神经无缝隙连接(gap junction,GJ)对肌痉挛的影响。方法:采用自体血脑内注入法制备大鼠内囊出血致肌痉挛模型,检测皮质运动诱发电位(Motor Evoked Potential,MEP),应用免疫组化方法观察脊髓前角运动神经元连接蛋白C_x32的改变。结果:大鼠内囊出血后病灶侧MEP波幅较对侧显著降低(P<0.01),且出血后1周病灶侧波幅较出血前显著降低(P<0.01);MEP潜伏期显著延长(P<0.01)。脑出血后第1周,左侧脊髓灰质前角GJ蛋白C_x32显著升高,同时动物肌痉挛状态明显加重。结论:内囊定向的脑出血模型引起内囊损伤侧MEP波幅明显降低、潜伏时延长,脊髓前角运动神经元GJ数量增多。
Aim: To investigate the spasticity resulting of motoneuron gap junction in rat spash'city model, changes of motor evoked potentials and the expression of connexin 32 in anterior horn motoneuron were observed following experimental cerebral hemorrhage. Methods: The arterial blood from rat tail artery was slowly injected into the hindlimb of the right capsule, and the spastic model of capsular hemiplegia rats was produced. MEPs were recorded from the gastrocnemius muscle, the connexin32 was observed with immunohistochemical method. Results:Following the right capsule-orientated hemorrhage the amplitude of MEP for the right sensomotor cortex was obviously decreased in contrast with those for the left ( P < 0.01), the latencies of MEP for the right sensorimotor cortex were significantly elongated in comparison with those for the left ( P < 0.01). At the first week after capsular hemorrhage, the expression of connexin32 in the left anterior horn of spinal cord for the right internal capsule was significandy increased compared with levels for pre- injury (P < 0.05) , and the degree of the spasticity in rat was elevated. Conclusion: Capsule-orientated hemorrhage may induce the amplitude of MEP for the injured side decreased obviously and the latencies of MEP elongated. These results show the functional state and injuried condition for corticospinal tract to a certain degree, it induces gap junction in anterior horn motoneuron to increase. This may be the important cause for the spasticity production.
出处
《中国临床神经科学》
2003年第1期46-48,共3页
Chinese Journal of Clinical Neurosciences
基金
第三军医大学校管课题(2001001)
关键词
脑出血
运动诱发电位
缝隙连接
肌痉挛
cerebral hemorrhage motor evoked potential gap junction spasticity
