The aim of present work is the investigation of mechanisms underlying ubiquitous form of short-term synaptic plasticity -facilitation. The end-plate currents were recorded at frog neuromuscular preparations. To examine facilitation we used paired-pulse paradigm (5 - 500 ms interval). At the normal Ringer paired-pulse facilitation (PPF) was described by sum of two exponentially decayed components - F1 and F2. F1 had larger amplitude and decayed to 100 ms, F2, less pronounced,- to 500 ms. In BAPTA-AM-treated (100 mkM) preparations both components were greatly reduced. In EGTA-AM (100 mkM) preparations F1 was slightly affected, F2 was absent. In case of "magnesium" solution F1 and F2 were more pronounced, the "early", most significant and short component (Fe) appeared. In BAPTA-AM preparations Fe was missed and both others were decreased. In EGTA-AM preparations Fe wasn't affected, F1 was shortened and F2 was completely oppressed. In Sr2+- containing (1 mM) as well as in extremely low Ca2+ (0.2 mM) solutions Fe was slightly decreased and F1 was strongly diminished. We concluded that Fe is caused by activity of phasic release site and/or changes of Ca channels kinetics. The F1 is caused by activation of additional high-affinity Ca-binding site. The mechanisms of F2 can include activation of another (third) Ca-binding site, use-dependent changes in Ca entry, etc.