Depletion of the Ca++-dependent releasable pool of glutamate in striatal synaptosomes associated with dendrotoxin-induced potassium channel blockade
| Autor: | L. Barbeito, J. Siciliano, F. Dajas |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
Potassium Channels Potassium Dendrotoxin Glutamic Acid chemistry.chemical_element Endogeny Biology Glutamates medicine Animals Biological Psychiatry Elapid Venoms Synaptosome Aspartic Acid Glutamate receptor Potassium channel blocker Glutamic acid Corpus Striatum Potassium channel Rats Psychiatry and Mental health Neurology chemistry Biophysics Calcium Neurology (clinical) Neuroscience Synaptosomes medicine.drug |
| Zdroj: | Journal of Neural Transmission. 80:167-179 |
| ISSN: | 1435-1463 0300-9564 |
| DOI: | 10.1007/bf01245118 |
| Popis: | 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-amino-pyridine 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 superfusing the synaptosomes with 50 microM D-ASP. Moreover, continuous superfusion of DTX (7 microM) to synaptosomes almost completely dumped the subsequent release of GLU and ASP stimulated by 20 mM K+. It is concluded that blockade of presynaptic 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. |
| Databáze: | OpenAIRE |
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