Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo. Academic Article uri icon


  • 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.

published proceedings

  • Nat Neurosci

altmetric score

  • 15.5

author list (cited authors)

  • Srinivasan, R., Huang, B. S., Venugopal, S., Johnston, A. D., Chai, H., Zeng, H., Golshani, P., & Khakh, B. S.

citation count

  • 353

complete list of authors

  • Srinivasan, Rahul||Huang, Ben S||Venugopal, Sharmila||Johnston, April D||Chai, Hua||Zeng, Hongkui||Golshani, Peyman||Khakh, Baljit S

publication date

  • January 2015