Calcium signaling in non‐excitable cells: Ca²⁺release and influx are independent events linked to two plasma membrane Ca²⁺entry channels

Abstract

The regulatory mechanism of Ca 2þ influx into the cytosol from the extracellular space in non-excitable cells is not clear.

Activation of Phosphatidylinositol-Linked D1-Like Receptor Modulates FGF-2 Expression in Astrocytes via IP3-Dependent Ca2+ Signaling

“…The initial spike of cytosol calcium, as showed in Figures 4 B and 5A, resulted from intracellular calcium release, whereas the late components of calcium fluctuations were extracellular calcium influx via IP3-mediated emptying of the intracellular Ca 2ϩ store. In agreement with our data, the Ca 2ϩ influx into the cytosol is reported to be triggered by the emptying of the IP3-sensitive calcium stores (Putney, 1990) which induces entry of Ca 2ϩ directly into the store, instead of into the cytosol, through a plasma membrane transient receptor potential channel (Chakrabarti and Chakrabarti, 2006). Thus, in the presence of IP3, the store is being emptied and directly refilled alternatively, giving rise to a transient phase of quantal oscillatory Ca 2ϩ release.…”

Characterization of calcium signaling pathways in human preadipocytes

“…5A). This suggests that RyRs were not expressed in human preadipocytes, which supports the notion that RyRs contribute to Ca 2þ release in excitable cells, but not in non-excitable cells (Chakrabarti and Chakrabarti, 2006 oscillations were inhibited by the PLC inhibitor U73122 (Fig. 3B) or the IP3Rs inhibitor 2-amino-ethoxydiphenyl borate (Fig.…”

Ryanodine and IP3 receptor-mediated calcium signaling play a pivotal role in neurological infrared laser modulation

“…NG108 were bathed in Ca 2þ -chelated buffer for 30 min before beginning ratiometric Ca 2þ imaging to partially deplete intracellular Ca 2þ out of the unstimulated cells. 52 The normal resting intracellular Ca 2þ concentration is between 50 and 100 nM, 53,54 but this exposure depleted it to 15 AE 3 nM [Fig 3(a)]. Shortly after beginning perfusion of cells with Ca 2þ -containing solution, the resting intracellular Ca 2þ concentration reached a normal 52 AE 3 nM due to a capacitive Ca 2þ entry mechanism.…”