Abstract
Astrocytes can exocytotically release the transmitter glutamate. Increased cytosolic Ca 2+ concentration is necessary and sufficient in this process. The source of Ca 2+ for the Ca 2+-dependent exocytotic release of glutamate from astrocytes predominately comes from endoplasmic reticulum (ER) stores with contributions from both inositol 1,4,5-trisphosphate- and ryanodine/caffeine-sensitive stores. An additional source of Ca 2+ comes from the extracellular space via store-operated Ca 2+ entry due to the depletion of ER stores. Here transient receptor potential canonical type 1 containing channels permit entry of Ca 2+ to the cytosol, which can then be transported by the store-specific Ca 2+-ATPase to (re)fill ER. Mitochondria can modulate cytosolic Ca 2+ levels by affecting two aspects of the cytosolic Ca 2+ kinetics in astrocytes. They play a role in immediate sequestration of Ca 2+ during the cytosolic Ca 2+ increase in stimulated astrocytes as a result of Ca 2+ entry into the cytosol from ER stores and/or extracellular space. As cytosolic Ca 2+declines due to activity of pumps, such as the smooth ER Ca 2+-ATPase, free Ca 2+ is slowly released by mitochondria into cytosol. Taken together, the trinity of Ca 2+ sources, ER, extracellular space and mitochondria, can vary concentration of cytosolic Ca 2+ which in turn can modulate Ca 2+-dependent vesicular glutamate release from astrocytes. An understanding of how these Ca 2+ sources contribute to glutamate release in (patho)physiology of astrocytes will provide information on astrocytic functions in health and disease and may also open opportunities for medical intervention.
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