A chloride channel blocker reduces acetylcholine uptake into synaptic vesicles at the frog neuromuscular junction.
A key mechanism for loading acetylcholine (ACh(+)) into synaptic vesicles uses energy to transport H(+) into the vesicle interior and then exchanges H(+) for ACh(+). This mechanism requires anions to follow the H(+) into the vesicles to prevent the building up of an overwhelming electrical gradient across the vesicle membrane. Frog nerve-muscle preparations were treated with hypertonic solution in which sodium gluconate was the major constituent, which substantially increases the sizes of the quanta by increasing their ACh(+) content. The Cl(-) channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) antagonized the increases in quantal size, so it seems likely that Cl(-) follows H(+) to prevent the buildup of a potential gradient across the vesicular membrane.
Van der Kloot
William
W
Department of Physiology and Biophysics, SUNY at Stony Brook, NY 11794-8661, USA. wkloot@aol.com
D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D018118:Chloride Channels / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D005942:Gluconates / Q000378:metabolism; D006859:Hydrogen / Q000378:metabolism; D006982:Hypertonic Solutions; D066298:In Vitro Techniques; D009045:Motor Endplate / Q000187:drug effects; D018482:Muscle, Skeletal / Q000378:metabolism*; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism*; D009579:Nitrobenzoates / Q000494:pharmacology*; D011894:Rana pipiens; D013572:Synaptic Vesicles / Q000187:drug effects* / Q000378:metabolism*
D018118:Chloride Channels; D005942:Gluconates; D006982:Hypertonic Solutions; D009579:Nitrobenzoates; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D006859:Hydrogen; D000109:Acetylcholine; C030691:gluconic acid