Abstract
Ca 2+ influx into presynaptic terminals via voltage-dependent Ca 2+ channels triggers fast neurotransmitter release as well as different forms of synaptic plasticity. Using electrophysiological and genetic techniques we demonstrate that presynaptic Ca 2+ entry through Ca v2.3 subunits contributes to the induction of mossy fiber LTP and posttetanic potentiation by brief trains of presynaptic action potentials while they do not play a role in fast synaptic transmission, paired-pulse facilitation, or frequency facilitation. This functional specialization is most likely achieved by a localization remote from the release machinery and by a Ca v2.3 channel-dependent facilitation of presynaptic Ca 2+ influx. Thus, the presence of Ca v2.3 channels boosts the accumulation of presynaptic Ca 2+ triggering presynaptic LTP and posttetanic potentiation without affecting the low release probability that is a prerequisite for the enormous plasticity displayed by mossy fiber synapses .
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