核黄素缺乏对鸡坐骨神经传导功能的影响

EFFECTS OF RIBOFLAVIN DEFICIENCY ON CONDUCT FUNCTION OF SCIATIC NERVE IN CHICKENS

采用人工半合成饲料 ,单因子诱发雏鸡核黄素缺乏症 ,成功地对不同处理组、不同时期、不同临床表现的活体鸡坐骨神经进行了电生理检测。结果表明 ,核黄素缺乏可使雏鸡坐骨神经传导速度明显减慢 ,减慢的程度与核黄素缺乏程度、临诊表现、神经损伤呈正相关。缺乏组、治疗组实验鸡的传导速度在任何时期均明显慢于同龄正常鸡 ,即使症状消失 ,也未恢复至正常 ,仍相差很远。表现卷趾或不卷趾麻痹的鸡 ,传导速度无明显差异。被检测病鸡中 ,76%的动作电位潜伏期延长。上述结果导致坐骨神经呈现不同程度麻痹。而髓鞘、轴突变性、ATP供给不足和神经发育受阻是造成传导速度减慢、动作电位潜伏期延长的主要原因。此外 ,随着年龄的增长 ( 10～ 38日龄 ) ,正常鸡坐骨神经传导速度逐渐加快 ,35m/s→ 66m/s,而核黄素缺乏鸡 ( 1 7mg/kg日粮 ,缺乏组 )则没有明显变化 ,10m/s→ 2 2m/s。

Riboflavin deficiency was experimentally induced in chickens,then the conduct velocity of sciatic nerve and the latency of action potential were successfully determined on live chickens at different treatments,ages and clinical symptoms.The results showed that dietary riboflavin deficiency could slow down,the conduct velocity of sciatic nerve of the affected chickens evidently with the alteration of enzyme activity and the occurrence of pathological changes,Which associated positively with the extents of riboflavin deficiency,clinical symptoms and nerve injuries.The conduct velocity in deficient group and treatment group at any ages was obviously slower than that of normal chickens of the same aged,although the symptoms disappeared,the velocity did not reture to normal,also no significant differences between curled toe paralysis and non curled toe paralysis.The latency of action potential from 76% affected chickens determined was prolonged.The above results led to nerve paralysis at the different extents.Demyelination,axon degeneration,ATP in short supply and nerve developmental disturbance were major causes of slowing down the conduct velocity and the prolonged latency of action potential.In addition,the velocity of normal chickens gradually increased,form 35 m/s to 66 m/s,while growing(10-38days),but no significant changes,from 10 m/s to 22 m/s,in deficient group.