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Regulatory role of PKC and CaMK II in depression of neurotransmitter secretion induced by presynaptic L-type Ca2+-current in newly formed motor synapsesдоклад на конференции
- Авторы: Балезина О.П., Богачева П.О.
- Международная Конференция : 7th FENS Forum of Neuroscience
- Даты проведения конференции: 2010
- Тип доклада: не указан
- Докладчик: не указан
- Место проведения: Amsterdam, Netherlands, Netherlands
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Аннотация доклада:
Increased activity of K+v-channels controlled by PKC may be the mechanism of Ca2+-dependent inactivation in newly formed synapses. Accordingly, we suggest that Ca2+-dependent inhibition of synaptic transmission in reinnervated junctions involves Ca2+ influx through L-type channels, which downregulates positive effects of CaMK II on neurotransmitter release and enhances PKC-dependent stimulation of K+v-channels activity, therefore leading to depression of synaptic activity.
- Добавил в систему: Богачева Полина Олеговна