Abstrakti
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.
Alkuperäiskieli | Englanti |
---|---|
Sivut | 264-8 |
Sivumäärä | 5 |
Julkaisu | FEBS Letters |
Vuosikerta | 353 |
Numero | 3 |
DOI - pysyväislinkit | |
Tila | Julkaistu - 24 lokak. 1994 |
OKM-julkaisutyyppi | A1 Julkaistu artikkeli, soviteltu |