Abstract
2,5-Diterbutyl-1,4-benzohydroquinone, a specific blocker of Ca 2+-ATPase pumps, increased acetylcholine release from an identified synapse of Aplysia, as well as from Torpedo and mouse caudate nucleus synaptosomes. Because 2,5-diterbutyl-1,4-benzohydroquinone does not change the presynaptic Ca 2+ influx, the enhancement of acetylcholine release could be due to an accumulation of Ca 2+ in the terminal. This possibility was further checked by studying the effects of 2,5-diterbutyl-1,4-benzohydroquinone on twin pulse facilitation, classically attributed to residual Ca 2+. While preventing the fast sequestration of Ca 2+ by presynaptic organelles, 2,5-diterbutyl-1,4-benzohydroquinone magnified both twin pulse facilitation observed under low extracellular Ca 2+ concentration and twin pulse dysfacilitation observed under high extracellular Ca 2+ concentration. Thus, it is concluded that 2,5-diterbutyl-1,4-benzohydroquinone, by preventing Ca 2+ buffering near transmitter release sites, modulates acetylcholine release. As 2,5-diterbutyl-1,4-benzohydroquinone was also shown to decrease by 50% the uptake of 45Ca 2+ by isolated synaptic vesicles, we propose that synaptic vesicles can control the presynaptic Ca 2+ concentration triggering the release of neurotransmitter.
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