Fig. 5: Small Ca²⁺ transients during sleep are derived from multiple sources of Ca²⁺.

A Representative photomicrographs showing that whisker stimulation induced small Ca²⁺ transients in IP₃R₂ knockout mice, as illustrated by increased fluorescence intensity. The scale bar is 10 µm. The lower panel shows typical traces of Ca²⁺ transients. B Statistical data show the comparison of whisker stimulation-induced changes in Ca²⁺ transients with agonists and in IP3R₂ knockout mice with different manipulations of blockers (**P < 0.001, one-way ANOVA, F (6, 232) = 54.57; spots show the averaged value in each mouse, n = 5 mice in each group, the data are shown as the mean ± SD). C A schematic diagram shows the intrinsic ion channels involved in the oscillation. Whisker stimulation-induced glutamate release from neurons affects astrocytes via mGluR (metabotropic glutamate receptor), and mGluR activates PLC (phospholipase C) to release IP3 (inositol trisphosphate) and DAG (diacylglycerol), which in turn activate TRP channels (transient receptor potential ion channels) and NCX (the Na⁺/Ca²⁺ exchanger) channels and thus Ca²⁺ influx. ATP, UTP, and FMRF in Mrg mice can also activate Gq receptors (G protein-coupled receptors) to activate PLC and release IP3 and DAG, thus inducing Ca²⁺ influx via TRP channels and NCX channels. Note: Kir4.1, an inwardly rectifying potassium (Kir) channel.