摘要
应用培养的骨胳肌细胞,以^(125)I-α-BTX作为N-AChR的特异性配基研究了氨基甲酸酯类药物和梭曼对N-AChR代谢的影响。结果表明,高浓度氨基甲酸酯类药物预处理培养肌细胞4h,N-AChR的膜降解减慢且膜参入加快,细胞膜表面N-AChR数增加。低浓度梭曼也使N-AChR数增加,对N-AChR代谢的改变与高浓度氨基甲酸酯的作用相一致。用嘌呤霉素抑制N-AChR蛋白合成后观察受体参入,结果提示梭曼可能是通过加快受体参入过程而不是通过合成受体来增加N-AChR的。
The effects of carbamates and soman on the metabolism of nicotinic acetylcholine receptors (N-AChR) in cultured skeletal muscle cells were studied by 125I-a-bungarotoxin (125I-a-BTX), a specific marker. It was indicated that N^AChR degradation process was inhibited and the incorperation rate of IshAChR and the number of N^AChR in the surface of the cell membrane were increased 4h after prertreatment of high concentrations of carbamates. The number of N-AChR was also increased after pre-treatment of low concentrations of soman, whose effects on N-AChR metabolism were similar to those of high concentrations of carbamates. The incorperation rate of N-AChR was observed by inhibiting the protein synthesis with puromysin, suggesting that soman may increase the number of N-AChR by increasing the incorperation of N-AChR instead of increasing the synthesis of N-AChR.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1991年第3期230-234,共5页
Academic Journal of Second Military Medical University
关键词
氨基甲酸酯
梭曼
胆碱能受体
cholinergic receptros
cholinesterase inhibitors
carbamates
soman
