NITRIC-OXIDE SYNTHASE IN RAT NEUROMUSCULAR-JUNCTIONS AND IN NERVE-TERMINALS OF TORPEDO ELECTRIC ORGAN - ITS ROLE AS REGULATOR OF ACETYLCHOLINE-RELEASE

The distribution of nitric oxide synthase on peripheral motor system w as studied using a specific antibody against the neuronal isoform of n itric oxide synthase (nNOS), The immunoreactivity for nNOS was detecte d on the sarcolemmal surface of muscle cells, in intramuscular axons a nd in neuromuscular synapses, At the neuromuscular junctions, ultrastr uctural immunolabeling demonstrated that nNOS immunoreactivity was loc alized mainly into the presynaptic nerve terminals as well as adjacent postsynaptic muscle membrane, Similar immunostaining pattern was pres ent in frog muscles and Torpedo electric organs, After chronic muscle denervation, nNOS immunoreactity at endplate level decreased during th e first week but it was upregulated after 30 days of denervation, In d enervated endplates, nNOS immunoreactivity was localized in the termin al Schwann cells covering the degenerated neuromuscular junctions wher eas nNOS was not detected in Schwann cells under normal conditions, In Torpedo synaptosomes, acetylcholine (ACh) release elicited by potassi um depolarization was inhibited by NO donors such as sodium nitropruss ide, In contrast, application of inhibitors of NOS activity, aminoguan idine (AMG) and N-omega-Nitro-L-arginine methyl esther (L-NAME) increa sed acetylcholine release, These results indicate that nNOS is present at the motor nerve terminals in a variety of vertebrates and that it may be involved in the physiological modulation of ACh release and in the regulation of muscle response to nerve injury. (C) 1998 Wiley-Liss , Inc.