Abstract
Dendritic spines are believed to be micro-compartments of Ca(2+) regulation. In a recent study, it was suggested that the ubiquitous and evolutionarily conserved Ca(2+) sensor, calmodulin (CaM), is the first to intercept Ca(2+) entering the spine and might be responsible for the fast decay of Ca(2+) transients in spines. Neuronal calcium sensor (NCS) and neuronal calcium-binding protein (nCaBP) families consist of Ca(2+) sensors with largely unknown synaptic functions despite an increasing number of interaction partners. Particularly how these sensors operate in spines in the presence of CaM has not been discussed in detail before. The limited Ca(2+) resources and the existence of common targets create a highly competitive environment where Ca(2+) sensors compete with each other for Ca(2+) and target binding. In this review, we take a simple numerical approach to put forth possible scenarios and their impact on signaling via Ca(2+) sensors of the NCS and nCaBP families. We also discuss the ways in which spine geometry and properties of ion channels, their kinetics and distribution, alter the spatio-temporal aspects of Ca(2+) transients in dendritic spines, whose interplay with Ca(2+) sensors in turn influences the race for Ca(2+).