Temporal and Spatial Changes in Ca2 Concentration

When the membrane channels and the intracellular release channels are activated, only brief pulses of Ca2+ are produced, since these channels have short open times. These elementary Ca2+ signals are localized around the channels and provide local control of many physiological reactions such as activation of other ion channels and nuclear-specific Ca2+ signals. The coordinated recruitment of many elementary Ca2+ release and entry channels allows the formation of global Ca2+ signals that persist 

Various feedback mechanisms exist that ensure a decrease in Ca2+ concentration and concomitant peak and wave formation under conditions of constant exposure to stimulatory signals. One example is provided by the Ca2+-dependence of subtypes of RGS proteins (Ishii et al., 2002) that can attenuate and shut down G protein-mediated signals. One of the effectors of Gq proteins is phospholipase Cfi, which stimulates Ca2+ release by InsP3 formation. Activation of Gq proteins by G protein-coupled receptors can be terminated by RGS proteins, subtypes of which are Ca2+/ calmodulin dependent. These RGS proteins are stimulated under conditions of high Ca2+ and will therefore inhibit further activation of phospholipase Cfi and the induction of InsP3/Ca2+ signals. 

How the frequency of an oscillating Ca2+ signal is decoded or integrated and incorporated into specific biochemical reactions is not understood. There is evidence that the CaM kinase II (see Section 7.5.2) is involved in decoding repetitive Ca2+ signals (De Koninck and Schulmann, 1998). 

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