Rises in free [Ca2+](i) in response to various tetanic stimuli (Ca2+ transi
ent) 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 H
z and decayed in a three-exponential manner, in which the fast component wa
s predominant. The plateau and fast component of the Ca2+ transient were el
evated infralinearly with an increase in tetanus frequency. Computer simula
tion showed that the Ca2+ transients estimated from fluorescence changes fa
ithfully 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 transmit
ter release and the time constant of the former. A fast Ca2+ chelator, BAPT
A, 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 t
hree components, in which the rate of the fast component is equivalent to t
hat of free Ca2+ diffusion. The residual Ca2+ in the nerve terminals after
stimulation accounts for the fast component of facilitation.