Nitric oxide synthase in rat neuromuscular junctions and in nerve terminals of Torpedo electric organ: its role as regulator of acetylcholine release.

摘要: The distribution of nitric oxide synthase on peripheral motor system was studied using a specific antibody against the neuronal isoform (nNOS). immunoreactivity for nNOS detected sarcolemmal surface muscle cells, in intramuscular axons and neuromuscular synapses. At junctions, ultrastructural immunolabeling demonstrated that localized mainly into presynaptic nerve terminals as well adjacent postsynaptic membrane. Similar immunostaining pattern present frog muscles Torpedo electric organs. After chronic denervation, immunoreactity at endplate level decreased during first week but it upregulated after 30 days denervation. In denervated endplates, terminal Schwann cells covering degenerated junctions whereas not under normal conditions. synaptosomes, acetylcholine (ACh) release elicited by potassium depolarization inhibited NO donors such sodium nitroprusside. contrast, application inhibitors NOS activity, aminoguanidine (AMG) N(omega)-Nitro-L-arginine methyl esther (L-NAME) increased release. These results indicate is variety vertebrates may be involved physiological modulation ACh regulation response to injury.