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• W1985238280 endingPage "268" @default.
• W1985238280 startingPage "264" @default.
• W1985238280 abstract "Ca2+ entry is a prerequisite for both exocytosis and the phosphorylation of synapsin I and MARCKS proteins in mammalian cerebrocortical synaptosomes. The novel spider toxin Aga-GI completely blocks KCl-evoked glutamate exocytosis but only partially inhibits KCl-evoked cytoplasmic Ca2+ elevations, thus revealing at least two pathways for KCl-induced Ca2+ entry. Aga-GI completely attenuates KCl-induced phosphorylation of synapsin I and MARCKS proteins. We therefore conclude that both exocytosis and the phosphorylation of synapsin I and MARCKS proteins are specifically coupled to Ca2+ entry via a subset of voltage dependent Ca2+ channels at the nerve terminal which are sensitive to Aga-GI." @default.
• W1985238280 created "2016-06-24" @default.
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• W1985238280 creator A5031762065 @default.
• W1985238280 creator A5063451537 @default.
• W1985238280 creator A5068969195 @default.
• W1985238280 date "1994-10-24" @default.
• W1985238280 modified "2023-09-24" @default.
• W1985238280 title "Phosphorylation of synapsin I and MARCKS in nerve terminals is mediated by Ca²⁺entry via an Aga-GI sensitive Ca²⁺channel which is coupled to glutamate exocytosis" @default.
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• W1985238280 doi "https://doi.org/10.1016/0014-5793(94)01061-7" @default.
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• W1985238280 hasPublicationYear "1994" @default.
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