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Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo. | Academic Article individual record
abstract

Intracellular Ca(2+) signaling is considered to be important for multiple astrocyte functions in neural circuits. However, mice devoid of inositol triphosphate type 2 receptors (IP3R2) reportedly lack all astrocyte Ca(2+) signaling, but display no neuronal or neurovascular deficits, implying that astrocyte Ca(2+) fluctuations are not involved in these functions. An assumption has been that the loss of somatic Ca(2+) fluctuations also reflects a similar loss in astrocyte processes. We tested this assumption and found diverse types of Ca(2+) fluctuations in astrocytes, with most occurring in processes rather than in somata. These fluctuations were preserved in Ip3r2(-/-) (also known as Itpr2(-/-)) mice in brain slices and in vivo, occurred in end feet, and were increased by G protein-coupled receptor activation and by startle-induced neuromodulatory responses. Our data reveal previously unknown Ca(2+) fluctuations in astrocytes and highlight limitations of studies that used Ip3r2(-/-) mice to evaluate astrocyte contributions to neural circuit function and mouse behavior.

author list (cited authors)
Srinivasan, R., Huang, B. S., Venugopal, S., Johnston, A. D., Chai, H., Zeng, H., Golshani, P., & Khakh, B. S.
publication date
2015
published in
keywords
  • AnimalsAstrocytesCalcium SignalingCrosses, GeneticFemaleFluorescent DyesHippocampusInositol 1,4,5-Trisphosphate ReceptorsMaleMiceMice, TransgenicPrazosinReflex, StartleSoftware