Publications by authors named "O Yagasaki"

To clarify the mechanism of exocytosis in neurotransmitter release, the fusion of synaptic vesicles with presynaptic membranes prepared from rat brain synaptosomes and concomitant acetylcholine (ACh) release induced by fusion of them were studied in vitro. Fusion of the synaptic vesicles with presynaptic membranes was measured by a fluorescence-dequenching assay with octadecyl rhodamine B. Synaptic vesicles fused with presynaptic membranes which had been pretreated with porcine phospholipase A2 (PLA2) in the presence of 20 microM Ca2+ and released ACh, whereas synaptic vesicles did not interact with non-pretreated membranes.

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In order to clarify the involvement of cyclic AMP-dependent protein kinase (protein kinase A) in acetylcholine (ACh) release from myenteric plexus of guinea pig ileum, the effect of H-89, a specific inhibitor of protein kinase A, on the ACh release was investigated. H-89 (0.1-10 microM) inhibited the spontaneous and nicotine-induced release of ACh in a concentration dependent manner.

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1. The effects of several conditions and agents on the twin-pulse facilitation of the release of transmitter at the mouse neuromuscular junction in low-Ca2+ high-Mg2+ bathing solutions were examined. 2.

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1. The effects of a reduction in temperature were examined on evoked and spontaneous release of transmitter quanta and on presynaptic negative signals, blocked by Cd2+, measured externally at neuromuscular junctions in mouse diaphragm muscles in low-Ca2+, high-Mg2+ Krebs-Ringer solutions. 2.

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The roles of metabolites of arachidonic acid in spontaneous and agonist-induced acetylcholine release from a longitudinal muscle preparation with myenteric plexus of guinea-pig ileum were studied. Indomethacin significantly decreased both spontaneous acetylcholine release and its release induced by nicotine and substance P. We had found that prostaglandin E2 (PGE2) partly reversed this inhibition.

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