Presynaptic effects of sodium bisulfite at the frog neuromuscular junction.
Both spontaneous and evoked transmitter release from the frog neuromuscular junction can be modified by application of sodium bisulfite, a reagent specific for disulfide bonds. An increase in miniature endplate frequency is produced that is not dependent on external calcium, sodium, or presynaptic terminal depolarization. The increased release can be halted by application of the sulfhydryl oxidizing agent DTNB. The response of bisulfite can be prevented by prior treatment of the endplate with acetylcholine or an anticholinesterase. It is concluded that bisulfite produces its effects by acting on a protein in the presynaptic membrane that is involved in regulation of transmitter release.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D004228:Dithionitrobenzoic Acid / Q000494:pharmacology; D005399:Fishes; D008564:Membrane Potentials / Q000187:drug effects; D008565:Membrane Proteins / Q000378:metabolism; D009045:Motor Endplate / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D011894:Rana pipiens; D013447:Sulfites / Q000494:pharmacology*; D013570:Synaptic Membranes / Q000187:drug effects
D008565:Membrane Proteins; D013447:Sulfites; D004228:Dithionitrobenzoic Acid; D000109:Acetylcholine; C009279:sodium bisulfite