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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Brain Res Rev. 2009 Dec 4;63(1-2):83–92. doi: 10.1016/j.brainresrev.2009.11.008

Figure 2.

Figure 2

Sources of cytosolic Ca2+ in vesicular release from astrocytes. Increase of cytosolic Ca2+ is sufficient and necessary to cause vesicular fusions and release of gliotransmitters. This process of regulated exocytosis requires the action of the ternary SNARE complex. Cytosolic Ca2+ accumulation could be caused by the entry of Ca2+ from the ER internal stores via IP3 and ryanodine receptors (IP3 and RyR). Store specific Ca2+-ATPase fills these stores, although ultimately this action requires Ca2+ entry from the extracellular space (ECS) through canonical type 1 transient receptor potential (TRPC1). Mitochondrial Ca2+ uptake is mediated by the uniporter, while free Ca2+within the mitochondrial matrix exits through the Na+/ Ca2+ exchanger and the mitochondrial permeability transition pore (MPTP). Drawing is not to scale.