摘要
目的观察大鼠实验性脑出血后皮层运动诱发电位(motorevokedpotential,MEP)和脊髓前角运动神经元中缝隙连接蛋白Cx32的改变。以了解脑出血后肌痉挛发生过程中脊髓运动神经元缝隙连接(gapjunction,GJ)对肌痉挛的影响。方法采用大鼠自体血缓慢注入右侧内囊后肢制备大鼠脑内囊出血致肌痉挛模型,应用电生理学方法检测皮层运动诱发电位,应用免疫组化方法观察脊髓前角运动神经元连接蛋白Cx32的改变。结果大鼠右侧内囊出血后右侧MEP波幅较左侧显著降低(P<0.01),出血1周以后病灶侧MEP波幅较出血前均显著降低(P<0.01);MEP潜伏时右侧显著延长,与左侧比较差异非常显著(P<0.01),内囊出血1周以后,MEP潜伏时均明显延长,与出血前比较差异显著(P<0.01)。脑出血后第1周,左侧脊髓灰质前角缝隙连接蛋白Cx32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,一定程度上反映了脊髓束的损伤情况和功能状态,与此同时使脊髓前角运动神经元缝隙连接数量增多,导致神经元兴奋性的同步作用增强,这可能是肌痉挛产生的重要原因。
Aim To investigate the effects on spasti city from motoneuron gap junction(GJ )in rat spasticity model,changes of m otor evoked potentials(MEPs )and the express of connexin 32in ante rior horn motoneuron were ob-served following experimental cere bral hemorrhage.Methods The arterial blood from rat tail artery was slowly injected into the hindlimb of the rig ht capsule,which induced pyramidal tr act to damage,and the spastic model o f capsular hemiplegia rats was produced.MEPs were recorded from the gastr oc-nemius muscle,and the connexin32wa s observed with immunohistochemica l method.Results Following the right capsule-orient ated hemorrhage the am-plitude of motor evoked potential fo r 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 we re significantly elongated in comparison with those for the left(P<0.01),moreover,the latencies for the rig ht after 1week post-hemorrhage were markedly prolonged as compared with prehemorrhage(P<0.01).At the first week after capsular hem orrhage,the express of connexin32in the left anterior horn of spinal cord for the right internal capsule w as significantly increased compared with levels for pre-injury(P<0.05),and the degree of the spasticity in rat wa s elevated.Conclusion Cap-sule-orientated hemorrhage may induce the amplitude of MEP for the injur ed side decreased obviously and the lat encies of MEP elongated.These show t he functional state and injured 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 p roduction.
出处
《中国临床康复》
CSCD
2003年第10期1508-1509,F002,共3页
Chinese Journal of Clinical Rehabilitation
基金
解放军第三军医大学校管课题(2001001)~~
