Astroglial Ca(2+) signaling is generated by the coordination of IP3R and store-operated Ca(2+) channels.

Astrocytes play key roles in the central nervous system and regulate local blood flow and synaptic transmission via intracellular calcium (Ca(2+)) signaling. Astrocytic Ca(2+) signals are generated by multiple pathways: Ca(2+) release from the endoplasmic reticulum (ER) via the inositol 1, 4, 5-trisphosphate receptor (IP3R) and Ca(2+) influx through various Ca(2+) channels on the plasma membrane. However, the Ca(2+) channels involved in astrocytic Ca(2+) homeostasis or signaling have not been fully characterized. Here, we demonstrate that spontaneous astrocytic Ca(2+) transients in cultured hippocampal astrocytes were induced by cooperation between the Ca(2+) release from the ER and the Ca(2+) influx through store-operated calcium channels (SOCCs) on the plasma membrane. Ca(2+) imaging with plasma membrane targeted GCaMP6f revealed that spontaneous astroglial Ca(2+) transients were impaired by pharmacological blockade of not only Ca(2+) release through IP3Rs, but also Ca(2+) influx through SOCCs. Loss of SOCC activity resulted in the depletion of ER Ca(2+), suggesting that SOCCs are activated without store depletion in hippocampal astrocytes. Our findings indicate that sustained SOCC activity, together with that of the sarco-endoplasmic reticulum Ca(2+)-ATPase, contribute to the maintenance of astrocytic Ca(2+) store levels, ultimately enabling astrocytic Ca(2+) signaling.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}