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Control of K(Ca) channels by calcium nano/microdomains Fakler B; Adelman JPNeuron 2008[Sep]; 59 (6): 873-81Transient elevations in cytoplasmic Ca(2+) trigger a multitude of Ca(2+)-dependent processes in CNS neurons and many other cell types. The specificity, speed, and reliability of these processes is achieved and ensured by tightly restricting Ca(2+) signals to very local spatiotemporal domains, "Ca(2+) nano- and microdomains," that are centered around Ca(2+)-permeable channels. This arrangement requires that the Ca(2+)-dependent effectors reside within these spatial boundaries where the properties of the Ca(2+) domain and the Ca(2+) sensor of the effector determine the channel-effector activity. We use Ca(2+)-activated K(+) channels (K(Ca)) with either micromolar (BK(Ca) channels) or submicromolar (SK(Ca) channels) affinity for Ca(2+) ions to provide distance constraints for Ca(2+)-effector coupling in local Ca(2+) domains and review their significance for the cell physiology of K(Ca) channels in the CNS. The results may serve as a model for other processes operated by local Ca(2+) domains.|Animals[MESH]|Calcium Signaling/*physiology[MESH]|Calcium/*physiology[MESH]|Central Nervous System/cytology/physiology[MESH]|Cytoplasm/metabolism[MESH]|Humans[MESH]|Membrane Microdomains/*physiology[MESH]|Neurons/metabolism[MESH]|Potassium Channels, Calcium-Activated/*metabolism[MESH]|Second Messenger Systems/*physiology[MESH] |
