Studies on the amphibian neuromuscular junction have indicated that N-type
calcium channels are the sole mediators of stimulus-evoked neurotransmitter
release. We show, via both presynaptic and postsynaptic voltage-clamp meas
urements, that dihydropyridine (DHP)-sensitive calcium channels also contri
bute to stimulus-evoked release at developing Xenopus neuromuscular junctio
ns. Whereas inhibition of postsynaptic responses by omega -conotoxin (omega
-Ctx) GVIA has been taken previously as evidence that only N-type channels
mediate transmitter release, we find that both N-type and DHP-sensitive ca
lcium currents are sensitive to this toxin. The unusual sensitivity of DHP-
sensitive calcium channels to omega -Ctx GVIA in presynaptic terminals rais
es the possibility that this channel type may have escaped detection in pre
vious physiological studies on adult frog neuromuscular junctions. Alternat
ively, the additional channel isoforms may be present only during early dev
elopment, when they may serve to strengthen collectively presynaptic releas
e during critical periods of synaptogenesis.