The increase in cytosolic calcium, [Ca2+]c, evoked with 50 mM KCl in cerebellar granule cells consists of four components; (1) a rapidly inactivating transient or spike; (2) a nifedipine-sensitive non-inactivating plateau; (3) an Aga-GI (spider toxin) sensitive non-inactivating plateau; (4) a residual non-inactivating plateau insensitive to nifedipine and Aga-GI. None of these components is blocked by synthetic arginine polyamine toxin, spermine, (+)-MK-801 hydrogen maleate, d(-)-2-amino-5-phosphonopentanoic acid or ω-conotoxin-GVIA. The proposed P-type channel antagonist, ω-agatoxin-IVA, has a limited but non-significant effect on the elevated plateau [Ca2+]c. L-type Ca2+ channels are localized primarily on the soma whereas the component of the plateau which is blocked specifically by Aga-GI is localized primarily on the cell neurites. The latter component is coupled to the exocytosis of endogenous glutamate evoked with 50 mM KCl.
- cerebellar granule cell
- glutamate exocytosis
- spider toxin Aga-GI
- voltage dependent calcium channel