Transmitter release is triggered by highly localized, transient increases in the presynaptic Ca2+ concentration ([Ca2+]). Rapidly decaying [Ca2+] elevations were generated using Ca2+ uncaging techniques, and [Ca2+] was measured with a low-affinity Ca2+ indicator in a giant presynaptic terminal, the calyx of Held, in rat brain slices. The rise time and amplitude of evoked excitatory postsynaptic currents (EPSCs) depended on the half-width of the fluorescence transient, which was predicted by a five−binding site model of a Ca2+ sensor having relatively high affinity (Kd13 M). Very fast [Ca2+] transients (half-width <0.5 ms) evoked EPSCs similar to those elicited by a single action potential (AP) in the same synapse. Triggering release with dual [Ca2+] transients of variable amplitudes demonstrated the supralinear transfer function of the sensor. The sensitivity of release to the time course of the [Ca2+] transient may contribute to mechanisms by which the presynaptic AP waveform controls synaptic strength.
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M). Very fast [Ca2+] transients (half-width <0.5 ms) evoked EPSCs similar to those elicited by a single action potential (AP) in the same synapse. Triggering release with dual [Ca2+] transients of variable amplitudes demonstrated the supralinear transfer function of the sensor. The sensitivity of release to the time course of the [Ca2+] transient may contribute to mechanisms by which the presynaptic AP waveform controls synaptic strength.
