What resolves this contention: Whether astrocytic IP3R2-dependent Ca2+ signalin…

What resolves this contention: Whether astrocytic IP3R2-dependent Ca2+ signaling is required for normal neuronal activity and behavior. Petravicz et al. 2014 report no deficits in Itpr2-/- mice using standard learning/memory assays, whereas the 2025 dual-color imaging study in vibrissa cortex reports Itpr2-/- mice exhibit reduced astrocytic Ca2+ activity and altered neuronal dynamics. / IP3R2-dependent astrocyte Ca2+ signaling is not a major modulator of neuronal excitability and synaptic or behavioral plasticity; Itpr2-/- mice show no measurable deficits across multiple learning and memory assays. / IP3R2-dependent astrocytic Ca2+ transients are critical for maintaining normal neuronal activity and task performance; Itpr2-/- mice show impaired signaling and behavioral consequences.