Abstract
Many fundamental calcium-dependent physiological processes are triggered by high local calcium levels that are established around the sites of calcium entry into the cell (channels). They are dubbed as calcium nanodomains but their exact profiles are still elusive. The concept of calcium nanodomains stems from a linear model of calcium diffusion and is only valid when calcium increases are smaller than the concentration of cytoplasmic buffers. Recent data indicates that much higher calcium levels cause buffer saturation. Therefore, I sought explicit solutions of a nonlinear reaction-diffusion model and found a dichotomous solution. For small fluxes, the steady state calcium profile is quasi-exponential, and when calcium exceeds buffer concentration a spatial periodicity appears. Analytical results are supported by Monte-Carlo simulations. I also imaged 1D- and radial calcium distributions around single α-synuclein channels in cell-free conditions. Measured Ca profiles are consistent with theoretical predictions. I propose that the periodic calcium patterns may well arise under certain conditions and their specific functional role has to be established.
Highlights
Many fundamental calcium-dependent physiological processes are triggered by high local calcium levels that are established around the sites of calcium entry into the cell
rapid binding approximation (RBA) application to experiments made in the same neuronal type, gave values of the intrinsic model parameter κ ≈ Bo/Kd that vary by almost two orders of magnitude as summarized in[10]
The RD problem for calcium and a single buffer are given by the two partial ordinary differential equations (PDE)
Summary
Many fundamental calcium-dependent physiological processes are triggered by high local calcium levels that are established around the sites of calcium entry into the cell (channels). RBA application to experiments made in the same neuronal type, gave values of the intrinsic model parameter κ ≈ Bo/Kd that vary by almost two orders of magnitude as summarized in[10] This may merely manifest the fact that Ca reaction-diffusion systems are overdetermined, making it difficult to establish a molecular identity of Ca buffers in each particular case. RBA is not appropriate for considering the fate of Ca immediately after its exit from the single channel This was first recognized by Neher[12] and represents a cornerstone of the concept of Ca nanodomains as reviewed in[13,14]. Neher used a simple linear model and considered steady state calcium profiles around a single calcium channel generated by the radial diffusion.
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