Unraveling ChR2-driven stochastic Ca2+ dynamics in astrocytes: A call for new interventional paradigms
Fig 1
Schematic of the biophysical model.
A model for a ChR2-expressing astrocyte is presented, accounting for: 1) Ca2+ release from the endoplasmic reticulum (ER) into the cytosol via the IP3R clusters, 2) Phospholipase-C δ1 (PLCδ1) mediated production of IP3, 3) capacitive calcium entry (CCE) via the store operated calcium channel (SOC), 4) passive leak from the ER to the cytosol (Jleak), 5) replenishment of ER stores via sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) pump, 6) extrusion of Ca2+ by plasma membrane Ca2+ ATPase (PMCA) pump into the extracellular (EC) space, 7) passive leak (Jin) into the cytosol from the EC space, and 8) Ca2+ buffering by endogenous buffer proteins. In astrocytic network simulations (bottom panel), each cell is connected to its neighboring cells though Ca2+ and IP3 permeable gap junctions, indicated as and
, respectively, and a central region (blue shaded box) is stimulated with light. A 4-state model [closed states (c1 and c2) in red and open states (o1 and o2) in blue] is used to represent ChR2 gating dynamics. The blue light (λ = 470 nm) stimulation paradigm used to open ChR2, leading to a Ca2+ influx (JChR2), is characterized by pulse period (T) and pulse width (δ).
