Abstract
The drug 2-(4-phenylpiperidino)cyclohexanol (AH5183), which potently inhibits the active transport of acethylcholine (ACh) into synaptic vesicles, was used as pharmacological tool to study the functional role of synaptic vesicles in quantal transmitter release. Using microelectrode recording techniques, miniature endplate potentials (meps) and nerve-evoked endplate potentials (epps) were recorded from cutaneous pectoris neuromuscular junctions in low Ca 2+/high Mg 2+ Ringer solution, and in normal Ringer with added d-tubocurraine ( d-TC). Stimulation in the presence of AH5183 caused a 40% reduction in quantal size (mepp amplitude), depressed tetanic potentiation, and decreased the number of quanta released with each nerve impulse in the presence of d-TC. All of these effects prepared gradually and only after extended stimulation of the nerve, during which several hundred thousand quanta were released. Consequently, these findings suggest a serial one-time usage of vesicles, with little or no re-entry of recycled vesicles until after a large fraction of the original vesicles has been exhausted. The results primarily show that filling of synaptic vesicles with ACh is crucial for sustaining synaptic transmission, and gives further evidence that the ACh released by nerve impulses originates from these organelles.
Published Version
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