Voltage-dependent Ca2+ channels are considered as molecular trigger el
ements for signal transmission at chemical synapses. Due to their cent
ral role in this fundamental process, function and pharmacology of pre
synaptic Ca2+ channels have recently been the subject of extensive exp
loration employing various experimental techniques. Several lines of e
vidence indicate that, at nerve terminals in higher vertebrates, the e
voked influx of Ca2+ -ions is mainly mediated by Ca2+ channels of the
P-type. The stringent regulation of presynaptic Ca2+ channels is suppo
sed to be involved in fine-tuning the efficiency of synaptic transmiss
ion. Intrinsic control mechanisms, such as voltage- or Ca2+-dependent
inactivation, or modulation of channel activity, either by G-proteins
directly or via phosphorylation by protein kinases, may be of particul
ar functional importance.