Depletion of the Ca++-dependent releasable pool of glutamate in striatal synaptosomes associated with dendrotoxin-induced potassium channel blockade
- Cite this article as:
- Barbeito, L., Siciliano, J. & Dajas, F. J. Neural Transmission (1990) 80: 167. doi:10.1007/BF01245118
The presynaptic actions of the potassium channel blocker Dendrotoxin (DTX) on the Ca+2-dependent release of endogenous glutamate (GLU) and aspartate (ASP) have been tested in synaptosome-enriched preparations from rat striatum.
24 hours after the intrastriatal administration of DTX the K+-evoked release of GLU and ASP from the striatal synaptosomes was decreased by 40–45%. No changes in the total synaptosomal content of the amino acids were observed. Superfusion of immobilized synaptosomes with DTX or 4-aminopyridine resulted in a dose-dependent increase in the basal outflow of GLU and ASP. The release of GLU stimulated by DTX was Ca+2-dependent and was not abolished by supervising the synaptosomes with 50 μM D-ASP. Moreover, continous superfusion of DTX (7 μM) to synaptosomes almost completely dumped the subsequent release of GLU and ASP stimulated by 20mM K+. It is concluded that blockade of presyanptic K+ channels by DTX leads to a massive release of the transmitter pool of GLU (and possible also ASP) from isolated nerve terminals and to a depletion of the amino acid releasable pool.