Aas P, Malmei T, Fonnum F
Pharmacol Toxicol. 1987 Mar;60(3):206-9. doi: 10.1111/j.1600-0773.1987.tb01734.x.
The in vitro exposure of rat bronchial smooth muscle to the acetylcholinesterase inhibitor soman (0-[1,1,2-trimethylpropyl]-methylphosphonofluoridate) reduced the potassium (51 mM) evoked release of 3H-acetylcholine (3H-ACh). Exposure to 1.0 and 100 microM soman for 15 min inhibited the acetylcholinesterase (AChE) activity completely and reduced the potassium evoked release by 23.1% and 34.4% respectively. In the presence of scopolamine (0.3 microM), however, there was a large enhancement (87.0%) of potassium evoked release during soman inhibited (100%) AChE-activity. Furthermore, soman (1.0 microM) did not reduce the spontaneous release of 3H-ACh. The results indicate that the presynaptic effect of soman is due to the enhanced concentration of ACh following AChE-activity inhibition in the synaptic region. This induces a stimulation of presynaptic muscarinic receptors and thereby modulation of the ACh release only during evoked release.