The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice and...The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice andrats.The effects of the three anti-cholinesterase agents on N-AChR weredifferent.Sarin did not act directly on N-AChR and cause a change in the numberof N-AChR.VX decreased the binding sites of the receptor by binding with N-AChRdirectly.The LD<sub>50</sub>was 0.054mg/kg in mousse.Soman increased the binding sites,e.g.1～1.5 LD<sub>50</sub>soman increased the number of N-AChR of mouse diaphragm by 25%.The peak increaseof N-AChR was reached 0.5 h after poisoning and could last 96h.The receptornumber was still 22% higher than that of the control on the fourth day aftersoman poisoning in rats.Soman mainly increased the number of extrasynapticN-AChR,leading to the enhancement of sensitivity of cholinergic effectors toacetylcholine（ACh）,which is similar to the hypersensitiveness resulting fromdenervation.These findings are of significance in probing the receptor mecha-nisms and treatment of soman poisoning.展开更多
Autoradiography of nicotinic acetytcholine receptors(N-ACHR)with the application ofhistochemical staining location of cholinesterase was used to observe the effect of soman onjunctional and extrajunctional N-AChR.Test...Autoradiography of nicotinic acetytcholine receptors(N-ACHR)with the application ofhistochemical staining location of cholinesterase was used to observe the effect of soman onjunctional and extrajunctional N-AChR.Testing with the diaphragms and extensor digitorum longusmuscles of mice and rats,we found that soman mainly increased the number of extrajunctionalN-AChR.It did not alter the number of junctional N-AChR significantly,nor did it have any pro-nouneed effects on the gtycoprotein property and isoelectfic point(pI)of junctional andextrajunctional N-AChR.The change of extrajunctional N-AChR number caused by somanis similar to the phenomenon of increased extrajunctional N-AChR number and sensitivity resultingfrom denervation,but the mechanism of action is different from the latter.The increase ofN-AChR number is one of the important characteristics of soman poisoning which make it differ-ent from other nerve agents.To maintain the metabofic balance of N-AChR may be an importantnew approach to the treatment of soman poisoning.展开更多
文摘The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice andrats.The effects of the three anti-cholinesterase agents on N-AChR weredifferent.Sarin did not act directly on N-AChR and cause a change in the numberof N-AChR.VX decreased the binding sites of the receptor by binding with N-AChRdirectly.The LD<sub>50</sub>was 0.054mg/kg in mousse.Soman increased the binding sites,e.g.1～1.5 LD<sub>50</sub>soman increased the number of N-AChR of mouse diaphragm by 25%.The peak increaseof N-AChR was reached 0.5 h after poisoning and could last 96h.The receptornumber was still 22% higher than that of the control on the fourth day aftersoman poisoning in rats.Soman mainly increased the number of extrasynapticN-AChR,leading to the enhancement of sensitivity of cholinergic effectors toacetylcholine（ACh）,which is similar to the hypersensitiveness resulting fromdenervation.These findings are of significance in probing the receptor mecha-nisms and treatment of soman poisoning.
文摘Autoradiography of nicotinic acetytcholine receptors(N-ACHR)with the application ofhistochemical staining location of cholinesterase was used to observe the effect of soman onjunctional and extrajunctional N-AChR.Testing with the diaphragms and extensor digitorum longusmuscles of mice and rats,we found that soman mainly increased the number of extrajunctionalN-AChR.It did not alter the number of junctional N-AChR significantly,nor did it have any pro-nouneed effects on the gtycoprotein property and isoelectfic point(pI)of junctional andextrajunctional N-AChR.The change of extrajunctional N-AChR number caused by somanis similar to the phenomenon of increased extrajunctional N-AChR number and sensitivity resultingfrom denervation,but the mechanism of action is different from the latter.The increase ofN-AChR number is one of the important characteristics of soman poisoning which make it differ-ent from other nerve agents.To maintain the metabofic balance of N-AChR may be an importantnew approach to the treatment of soman poisoning.
