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The presynaptic calcium current (IpCa) was recorded from the calyx of Held in rat brainstem slices using the whole-cell patch clamp technique. 2. Tetanic activation of IpCa by 1 ms depolarizing voltage steps markedly enhanced the amplitude of IpCa. Using a paired pulse protocol, the second (test) response was facilitated with inter-pulse intervals of less than 100 ms. The facilitation was greater at shorter intervals and was maximal (about 20%) at intervals of 5-10 ms. 3. When the test pulse duration was extended, the facilitation was revealed as an increased rate of IpCa activation. From the current-voltage relationship measured at 1 ms from onset, facilitation could be described by a shift in the half-activation voltage of about -4 mV. 4. IpCa facilitation was not attenuated when guanosine-5'-O-(3-thiotriphosphate) (GTPgammaS) or guanosine-5'-O-(2-thiodiphosphate) (GDPbetaS) was included in the patch pipette, suggesting that G-proteins are not involved in this phenomenon. 5. On reducing Ca2+o, the magnitude of facilitation diminished proportionally to the amplitude of IpCa. Replacement of Ca2+o by Ba2+ or Na+, or buffering of Ca2+i with EGTA or BAPTA attenuated IpCa facilitation. 6. We conclude that repetitive presynaptic activity can facilitate the presynaptic Ca2+ current through a Ca2+-dependent mechanism. This mechanism would be complementary to the action of residual Ca2+ on the exocytotic machinery in producing activity-dependent facilitation of synaptic responses.
Cuttle et al. (Sun,) studied this question.