EN
Excessive activation of glutamatergic neurons in course of different encephalopathies is accompanied by marked increase of zinc concentration in the synaptic cleft. This cation is co-released with glutamate and subsequently taken up by cholinergic and other postsynaptic elements through ZIP transporters, NMDA and other voltage dependent Ca-channels. On the other hand, Zn distribution and clearance from cellular compartments is executed by multiple Zn-transporters (ZnT). The aim of this work was to investigate how variable levels of Zn in extracellular space affect its accumulation in cholinergic cells and their functions. Acute, 30 min exposure of differentiated and nondifferentiated SN56 cells to increasing concentrations of Zn yielded concave up, non saturable, super imposable accumulation plots. At 0.15 mM extracellular concentration, intracellular accumulation of Zn was about 60 nmol/mg protein. On the other hand, after 24 h cell culture with same Zn concentration its intracellular level was found to be equal to 6 nmol/mg protein, only. Atypical shape of concentration-dependent plots of Zn accumulation might be explained by the coexistence in cholinergic cell plasma membranes low density, high-affi nity and high density low affi nity Zn-transporting sites. On the other hand, time-dependent decrease of Zn accumulation might result from an adaptative increase of density of one of ZnT proteins, presumably ZnT4, thereby protecting cells against Zn overload. Supported by MNiSW grants NN401 2333 33 and P05A 110 30