Symposium 6

Intracellular calcium increase is believed as the main trigger for astrocyte functions modulating neuronal activities and vasculature. As in many other cell types, it is considered that astrocyte calcium is a multifunctional signal, and an appropriate spatial and temporal pattern of calcium increase is required to elicit a specific function. In addition to diverse calcium release patterns (transient, sustained and oscillatory) following G-protein coupled receptor activation by neurotransmitters, astrocyte is known to show unique calcium behaviors, including intrinsic calcium oscillation, intercellular calcium wave propagation, mechanically-induced calcium increase and reversal of sodium-calcium exchanger. And expressions of calcium-regulating receptors and ion channels are known to change depending on developmental and pathological states of astrocyte. Therefore astrocyte calcium is supposed to reflect not only neurotransmitter concentration, but also metabolic, ionic and physical environment, as well as astrocyte states and network. In our studies using cultured astrocytes, neurotransmitter-induced calcium oscillation was shown to require appropriate growth factor/cytokine treatment and neurotransmitter concentration, supporting the notion that astrocyte senses environmental parameters and determine its calcium behavior and following function. In our preliminary observation of astrocyte calcium behavior in normal and pathological brain tissue preparations, astrocyte changes its responsibility to neurotransmitters and frequency of intrinsic activities during pathological activation processes, and evoked and intrinsic activities interfere each other. These flexibilities of calcium behavior propose switching of astrocyte calcium regulatory mechanism and function in brain physiology and pathology.