Visualization of astrocytic intracellular Ca2+ mobilization.

Astrocytes generate robust intracellular Ca2+ concentration changes (Ca2+ signals), which are assumed to regulate astrocytic functions that play crucial roles in the regulation of brain functions. One frequently used strategy for exploring the role of astrocytic Ca2+ signalling is the use of mice deficient in the type 2 inositol 1,4,5-trisphosphate receptor (IP3 R2). These IP3 R2-knockout (KO) mice are reportedly devoid of Ca2+ mobilization from the endoplasmic reticulum (ER) in astrocytes. However, they have shown no functional deficits in several studies, causing a heated debate as to the functional relevance of ER-mediated Ca2+ signalling in astrocytes. Recently, the assumption that Ca2+ mobilization from the ER is absent in IP3 R2-KO astrocytes has been re-evaluated using intraorganellar Ca2+ imaging techniques. The new results indicated that IP3 R2-independent Ca2+ release may generate Ca2+ nanodomains around the ER, which may help explain the absence of functional deficits in IP3 R2-KO mice.