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Delayed increase of acetylcholine quantal size induced by the activity-dependent release of endogenous cgrp but not atp in neuromuscular junctionsстатья
- Авторы: Bogacheva Polina, Balezina Olga
- Журнал: Synapse
- Год издания: 2020
- Издательство: John Wiley & Sons Inc.
- Местоположение издательства: United States
- DOI: 10.1002/syn.22175
- Аннотация: At mouse motor synapses tetanic neuromuscular activity (30 Hz, 2 min) led to a delayed posttetanic potentiation of amplitude and duration of spontaneous miniature endplate potentials (MEPPs). Microelectrode recordings of MEPPs before and after nerve stimulation showed an increase in MEPP amplitude and time course by 30% and 15%, respectively, without a change in frequency. Peak effect was detected 20 min after tetanic activity and progressively faded throughout the next 40 min of recording. The revealed potentiation of MEPPs was fully preserved in preparations from pannexin 1 knockout mice. This means, that myogenic ATP released via pannexin 1 channels from contracting muscle fibers is not likely to participate in the described phenomenon. But posttetanic potentiation of MEPPs was fully prevented by the competitive antagonist of calcitonin gene-related peptide (CGRP) receptors CGRP8-37, the ryanodine receptor inhibitor ryanodine and by the vesicular acetylcholine transporter inhibitor vesamicol. It is suggested that the combination of intensive synaptic and contractile activity in neuromuscular junctions is required to induce Ca2+-dependent exocytosis of endogenous CGRP. The accumulation of CGRP in the synaptic cleft and its presynaptic activity may induce posttetanic potentiation of MEPP amplitude due to CGRP-stimulated acetylcholine loading into vesicles and subsequent increase of quantal size.
- Добавил в систему: Богачева Полина Олеговна