Ultrastructural Localization of Calcium at Synapses and Modulatory Interactions with Gangliosides

Abstract

In 1975/76 we published the functional hypothesis of an involvement of sialoglycomacromolecules, especially gangliosides, in the process of synaptic transmission, including memory formation (Rahmann, 1976; Rahmann et al., 1975; 1976). In our proposal it had been discussed that due to the ability of ganglioside-bound negatively charged sialic acids to form labile complexes together with Ca²⁺-ions, these glycosphingolipids are assumed to act as modulatory compounds for the Ca²⁺-dependent release of transmitter substances at synapses. Since 1975 we have been able to add to this hypothesis extensive experimental evidence (Rahmann, 1983; 1984; Rahmann et al., 1982; Probst et al., 1984). In the meantime it also had been supported by several other authors (Svennerholm, 1980; Tettamanti et al., 1980; Maggio et al., 1981; Veh and Sander, 1981; Leskawa and Rosenberg, 1981). The essential basis for our model is the well-known fact that almost every stage of neuronal activity, especially electrical responsiveness, depends on the presence of extra-cellular Ca²⁺. With regard to this, during recent years extensive experimental efforts were undertaken to establish subcellular Ca²⁺-deposits in the synaptic terminal. Rough endoplasmic reticulum, mitochondria and vesicles were determined as intracellular Ca²⁺-storage structures (McGraw et al., 1980; Chan et al., 1983). The electronmicroscopical methods used until now, however, failed to establish extra-cellular deposits of Ca²⁺.