Abstract
This study investigates the role of glycogenolysis in stimulated release of ATP as a transmitter from astrocytes. Within the last 20 years our understanding of brain glycogenolysis has changed from it being a relatively uninteresting process to being a driving force for essential brain functions like production of transmitter glutamate and homoeostasis of potassium ions (K+) after their release from excited neurons. Simultaneously, the importance of astrocytic handling of adenosine, its phosphorylation to ATP and release of some astrocytic ATP, located in vesicles, as an important transmitter has also become to be realized. Among the procedures stimulating Ca2+-dependent release of vesicular ATP are exposure to such transmitters as glutamate and adenosine, which raise intra-astrocytic Ca2+ concentration, or increase of extracellular K+ to a depolarizing level that opens astrocytic L-channels for Ca2+ and thereby also increase intra-astrocytic Ca2+ concentration, a prerequisite for glycogenolysis. The present study has confirmed and quantitated stimulated ATP release from well differentiated astrocyte cultures by glutamate, adenosine or elevated extracellular K+ concentrations, measured by a luciferin/luciferase reaction. It has also shown that this release is virtually abolished by an inhibitor of glycogenolysis as well as by inhibitors of transmitter-mediated signaling or of L-channel opening by elevated K+ concentrations.
Highlights
This study investigates the role of glycogenolysis in stimulated release of ATP as a transmitter from astrocytes
An effect similar to that of ARL 67156 was caused by DAB, which might suggest that ecto-ATPase action requires glycogenolysis
They illustrate the effects of 100 μM glutamate, 100 μM adenosine or an elevation of the extracellular K + concentration by 45 mM
Summary
This study investigates the role of glycogenolysis in stimulated release of ATP as a transmitter from astrocytes. Among the procedures stimulating Ca2 + -dependent release of vesicular ATP are exposure to such transmitters as glutamate and adenosine, which raise intra-astrocytic Ca2 + concentration, or increase of extracellular K + to a depolarizing level that opens astrocytic L-channels for Ca2 + and thereby increase intra-astrocytic Ca2 + concentration, a prerequisite for glycogenolysis. The present study has confirmed and quantitated stimulated ATP release from well differentiated astrocyte cultures by glutamate, adenosine or elevated extracellular K + concentrations, measured by a luciferin/ luciferase reaction. It has shown that this release is virtually abolished by an inhibitor of glycogenolysis as well as by inhibitors of transmitter-mediated signaling or of L-channel opening by elevated K + concentrations
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