Autoradiography of nicotinic acetylcholine receptors (N-AChR) with the application of histochemical staining location of cholinesterase was used to observe the effect of soman on junctional and extrajunctional N-AChR. Testing with the diaphragms and extensor digitorum longus muscles of mice and rats, we found that soman mainly increased the number of extrajunctional N-AChR. It did pot alter the number of junctional N-AChR significantly, nor did it have any pronounced effects on the glycoprotein property and isoelectric point (pI) of junctional and extrajunctional N-AChR. The change of extrajunctional N-AChR number caused by soman is similar to the phenomenon of increased extrajunctional N-AChR number and sensitivity resulting from denervation, but the mechanism of action is different from the latter. The increase of N-AChR number is one of the important characteristics of soman poisoning which make it different from other nerve agents. To maintain the metabolic balance of N-AChR may be an important new approach to the treatment of soman poisoning.