Store-Dependent Entry of Ca2+ into Sensory Neurons of the Rat

We studied store-dependent (activated by depletion of the endoplasmic reticulum, ER, store) entry of Ca2+ from the extracellular medium into neurons of the rat spinal ganglia (small- and medium-sized cells; diameter, 18 to 36 µm). Activation of ryanodine-sensitive receptors of the ER in the studied neurons superfused by Tyrode solutions containing Ca2+ or with no Ca2+ was provided by application of 10 mM caffeine. The decay phase of caffeine-induced calcium transients in a Ca2+-containing solution was significantly longer than that in a Ca2+-free solution. This fact allows us to suppose that such a phenomenon is determined by Ca2+ entry into the neuron from the extracellular medium activated by caffeine-induced depletion of the ER store. Substitution of Ca2+-free extracellular solution by Ca2+-containing Tyrode solution, after depletion of the ER stores induced by applications of 100 nM ryanodine, 200 µM ATP, or 1 µM thapsigargin, resulted in increases in the concentration of intracellular Ca2+. These observations allow us to postulate that store-dependent Ca2+ entry into the studied neurons is activated after depletion not only of the inositol trisphosphate-sensitive ER store but also of the ryanodine-sensitive store. This entry also occurs after blocking of ATPases of the ER by thapsigargin. The kinetic characteristics of the rising phase of store-dependent Ca2+ entry induced by depletion of the ER stores under the influence of various agents are dissimilar; this can be related to different mechanisms of activation of such signals and/or to a compartmental organization of the ER.