Calcium dynamics in the extracellular space of mammalian neural tissue

In the brain, hundreds of intracellular processes are known to depend on ca lcium influx; hence any substantial fluctuation in external calcium ([Ca2+] (o)) is likely to engender important functional effects. Employing the know n scales and parameters of mammalian neural tissue, we introduce and justif y,a computational approach to the hypothesis that large changes in local [C a2+](o) will be part of normal neural activity. Using this model, we show t hat the geometry of the extracellular space in combination with the rapid m ovement of calcium through ionic channels can cause large external calcium fluctuations, up to 100% depletion in many cases. The exact magnitude of a calcium fluctuation will depend on I)the size of the consumption zone, 2) t he local diffusion coefficient of calcium, and 3) the geometrical arrangeme nt of the consuming elements, Once we have shown that using biologically re levant parameters leads to calcium changes, we focus on the signaling capac ity of such concentration fluctuations. Given the sensitivity of neurotrans mitter release to [Ca2+](o), the exact position and timing of neural activi ty will delimit the terminals that are able to release neurotransmitter. Ou r results indicate that mammalian neural tissue is engineered to generate s ignificant changes in external calcium,concentrations during normal activit y. This design:suggests that such changes play a role in neural information processing.