Amyloid pathology disrupts gliotransmitter release in astrocytes
Fig 4
Characterization of the astrocytic compartmental models with Aβ-induced molecular alterations.
(A) Peak amplitudes of IP3 generated by DHPG stimulation from control and an astrocytic compartment with altered mGluR function are fitted to Hill functions for estimating dissociation constants (kd). (B) Steady-state PMCA fluxes from control and Aβ-PMCA conditions fitted to Hill functions. (C) Resting cytosolic Ca2+, IP3, and ER Ca2+ levels in control and Aβ-conditions. (D) Representative heat maps of Ca2+ signaling from control and Aβ conditions stimulated with DHPG. (E) Peak amplitude of Ca2+ event evoked with different DHPG concentrations. (F) Rate of Ca2+ events evoked by different DHPG concentrations. (G) Percentage Ca2+ response evoked by DHPG stimulation is higher the presence of Aβ conditions. Error bars indicate the standard error of the mean computed from 6 independent sets of simulation trials.