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The resulting binding data was used to calculate buffer capacities for each simulated cell and analyzed as for the BLO data. Average buffer capacity was obtained for many cells and the values were plotted against SNR and CImax. The simulations produce values of buffer capacity that are less than the values obtained using BLO. The results suggest that the CImax obtained at physiological CImax values is more likely to result from the binding of endogenous, rather than exogenous proteins. This suggests that the binding of CBPs is an important contributor to buffering capacity in the cortex [8], [3]. The simulations suggest that the values of buffer capacity are strongly dependent on the interplay of diffusion constants and mean lifetimes of the buffer states, the number of simulated time steps, and the spatial and temporal variability of the experimental conditions. This result is consistent with the observed dependence of CImax on the extracellular concentration of calcium. First, the binding of endogenous CBPs is likely to occur at concentrations of calcium in the spine that are much lower than the concentration of calcium in the bulk of the cytosol where most of the calcium-dependent effector molecules are localized. The observed linear relationship between CImax and SNR is likely to be the result of the combined effects of the lower calcium concentrations in the spine and the increased buffering capacity of the CBPs, because the variance in calcium concentration in the spine is directly proportional to SNR. A detailed analysis of simulated spatial and temporal concentration fluctuations, including calcium buffering, will be required to determine the relative contributions of the different factors in the measured variability of buffer capacity. Because the main effect of diffusion is to shift the concentration profiles in the direction of free calcium, it may be difficult to accurately measure and account for changes in concentration profile using fluorescence time-lapse techniques. In addition, the emission of many fluorescently-tagged proteins is significantly attenuated in dendritic and axonal spines ([29], [31], [32]). In many cases it may not be possible to distinguish between the effects of binding protein diffusion and attenuation of the fluorescent signal. It is not certain which experimental technique is best suited to measuring the buffering capacities of different proteins. Compared to calcium imaging experiments that use fluorescence indicators, MCell simulations suggest that diffusion of CBPs may be a major factor in the observed buffering capacity. Mapping buffer capacity in vivo using either a fluorescent calcium indicator or MCell simulations, that preserve endogenous concentrations of calcium and the binding of CBPs, will be an important step in elucidating the role of calcium binding proteins in regulating cytosolic calcium concentrations. The influence of CBPs on the ratio of cytosolic to bulk free calcium is more complex and will require further investigation. The results of these studies will be used in conjunction with the detailed kinetic and pharmacological properties of various calcium binding proteins in order to make predictions about the likelihood of calcium binding proteins being involved in regulating spine calcium concentrations during different types of synaptic activity.
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