The effects of inhibitors of arachidonate metabolism on spontaneous and evoked endplate potentials at normal and crotoxin-treated frog neuromuscular junctions.
Aspirin (1 mM), a selective cyclooxygenase inhibitor, decreased endplate potential (e.p.p.) amplitude but did not affect either the biphasic changes in m.e.p.p. frequency or triphasic changes in e.p.p. amplitude induced by crotoxin. Nordihydroguaiaretic acid (30 microM), a dual inhibitor of cyclooxygenase and lipoxygenase pathways, increased e.p.p. amplitude but did not affect the characteristic changes in m.e.p.p. frequency and e.p.p. amplitude in response to crotoxin. The incidence of giant m.e.p.p.s was reduced by aspirin and increased by NDGA. Arachidonate metabolism is not a major factor in the induction of neurotoxicity by crotoxin at the frog neuromuscular junction.
Edwards
J
J
Biomedical Sciences Division, King's College London, U.K.
Hawgood
B J
BJ
Smith
I C
IC
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D001241:Aspirin / Q000494:pharmacology; D003439:Crotoxin / Q000633:toxicity*; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D009637:Masoprocol / Q000494:pharmacology; D009045:Motor Endplate / Q000187:drug effects*; D009469:Neuromuscular Junction / Q000187:drug effects*; D011896:Rana temporaria
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D009637:Masoprocol; D003439:Crotoxin; D001241:Aspirin