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- W2045900673 abstract "A post-stimulation synthesis of acetylcholine (ACh), its incorporation into a ‘stable-bound’ (vesicular) compartment and subsequent release, were compared in K+-stimulated synaptosomes, in the absence and presence of 10 μM AH5183. The drug depressed by 16% the net intrasynaptosomal formation of ACh from 1 μM [3H]choline (Ch) in the medium, by competitively inhibiting (Ki⋍20μM) the high-affinity Ch transport, but it had no direct effect on the intraterminal synthesis of ACh per se. The drug reduce of newly synthesized [3H]ACh into synaptic vesicles by 55% and subsequent K+-depolarization-induced release of [3H]ACh by 83%, although it had no effect on Ca2+ influx into synaptosomes. These results are consistent with the hypothesis that AH5183 blocks cholinergic neurotransmission presynaptically by interfering with recharging of synaptic vesicles with ACh. Since the reduction of ACh release in the presence of AH5183 had no direct effect on ACh synthesis, these results also suggest that the transmitter release is not prerequisite for enhancement of Ch uptake and ACh synthesis in stimulated nerve terminals." @default.
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- W2045900673 date "1986-10-01" @default.
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- W2045900673 title "Storage and release of acetylcholine in rat cortical synaptosomes: Effects ofd,l-2-(4-phenylpiperidino)cyclohexanol (AH5183)" @default.
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- W2045900673 doi "https://doi.org/10.1016/0006-8993(86)90174-5" @default.
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