Transmitter release at frog end-plate loaded with a Ca2+-chelator, BAPTA: hypertonicity and erythrosin B augment the release independently of internal Ca2+.

A Ca2+-chelator, bis-(aminophenoxy)ethane-tetraacetic acid (BAPTA) was loaded into the presynaptic nerve terminal of frog end-plate. The BAPTA-loaded preparation showed little facilitation. However, the facilitation reappeared upon addition of an ionophore, X-537A, supporting the view that the loss of facilitation was due to the Ca2+-buffering action of BAPTA. Both hypertonic conditions and erythrosin B increased both the size of end-plate potentials and frequency of miniature end-plate potentials without any recovery of facilitation at the BAPTA-loaded end-plate. This suggested that transmitter release was increased by both conditions with little change in internal Ca2+ concentration.