Ca²⁺ dynamics at the frog motor nerve terminal

Rises in free [Ca²⁺](i) in response to various tetanic stimuli (Ca²⁺ transient) in frog motor nerve terminals were measured by recording fluorescence changes of Ca²⁺ indicators and analyzed in relation to short- term synaptic plasticity. Ca²⁺ transients reached a plateau after 10-20 impulses at 100 Hz and decayed in a three-exponential manner, in which the fast component was predominant. The plateau and fast component of the Ca²⁺ transient were elevated infralinearly with an increase in tetanus frequency. Computer simulation showed that the Ca²⁺ transients estimated from fluorescence changes faithfully reflect the true changes in [Ca²⁺](i) except for the initial 20 ms. A slow Ca²⁺ chelator, EGTA, loaded into the nerve terminal, decreased the magnitude of both the fast and slow components of facilitation of transmitter release and the time constant of the former. A fast Ca²⁺ chelator, BAPTA, decreased the magnitude of fast facilitation but slightly increased its time constant. These results suggest that Ca²⁺ transients in the frog motor nerve terminals are primarily caused by Ca²⁺ entry and are dissipated by three components, in which the rate of the fast component is equivalent to that of free Ca²⁺ diffusion. The residual Ca²⁺ in the nerve terminals after stimulation accounts for the fast component of facilitation.