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The Journal of Neuroscience, May 25, 2005, 25(21):5127-5137; doi:10.1523/JNEUROSCI.1295-05.2005
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Cellular/Molecular
Presynaptic Ca2+ Requirements and Developmental Regulation of Posttetanic Potentiation at the Calyx of Held
Natalya Korogod, Xuelin Lou, andRalf Schneggenburger AG Synaptische Dynamik und Modulation and Abteilung Membranbiophysik, Max-Planck-Institut für Biophysikalische Chemie, D-37077 Göttingen, Germany
Large excitatory synapses in the auditory system, such as the calyx of Held, faithfully transmit trains of action potentials up to a frequency of a few hundred hertz, and these synapses are thought to display a limited repertoire of synaptic plasticity. Here, we show that brief trains of 100 Hz stimulation induce posttetanic potentiation (PTP) of transmitter release at the calyx of Held. In young rats [postnatal day 4 (P4) to P6], PTP could be induced with shorter 100 Hz trains compared with older age groups (P8-P10 and P12-P14), but the maximal amount of PTP was similar, with
200% of control EPSC amplitude. The size of the readily releasable pool of vesicles was not increased significantly during PTP. Bath application of the membrane-permeable Ca2+ chelator EGTA-AM suppressed PTP, indicating a role for presynaptic Ca2+ in PTP at the calyx of Held. Presynaptic Ca2+ imaging showed that the intracellular Ca2+ concentration, [Ca2+]i, was increased by 40-120 nM at the peak of PTP, and this "residual" [Ca2+]i decayed in parallel with PTP, with time constants in the range of 10-60 s. During whole-cell recording of the presynaptic calyx of Held, PTP was absent, and the decay of residual [Ca2+]i was strongly accelerated. The data show that the calyx of Held expresses a mechanism of transmitter release potentiation in which a small, sustained elevation of basal [Ca2+]i increases the transmitter release probability after trains of high-frequency stimulation.
Key words: synaptic plasticity; nerve terminal; transmitter release; release probability; calcium; imaging
Received July 22, 2004; revised April 14, 2005; accepted April 14, 2005.
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