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dc.contributor.authorGonzález Inchauspe, C.-
dc.contributor.authorMartini, F. J.-
dc.contributor.authorUchitel, O. D.-
dc.contributor.authorForsythe, Ian D.-
dc.identifier.citationJournal of Neuroscience, 2004, 24 (46), pp. 10379-10383-
dc.description.abstractCalcium channels of the P/Q subtype mediate transmitter release at the neuromuscular junction and at many central synapses, such as the calyx of Held. Transgenic mice in which α1A channels are ablated provide a powerful tool with which to test compensatory mechanisms at the synapse and to explore mechanisms of presynaptic regulation associated with expression of P/Q channels. Using the calyx of Held preparation from the knock-out (KO) mice, we show here that N-type channels functionally compensate for the absence of P/Q subunits at the calyx and evoke giant synaptic currents [approximately two-thirds of the magnitude of wild-type (WT) responses]. However, although evoked paired-pulse facilitation is prominent in WT, this facilitation is greatly diminished in the KO. In addition, direct recording of presynaptic calcium currents revealed that the major functional difference was the absence of calcium-dependent facilitation at the calyx in the P/Q KO animals. We conclude that one physiological function of P/Q channels is to provide additional facilitatory drive, so contributing to maintenance of transmission as vesicles are depleted during high throughput synaptic transmission.-
dc.description.sponsorshipThis work was supported by Wellcome Trust Grant 068941/Z/02/Z, Agencia Nacional de Promocion Cientıfica y Tecnologica Grant 6220, and Universidad de Buenos Aires Ciencia y Technica Grant X171.W-
dc.publisherSociety for Neuroscience-
dc.rightsCreative Commons Attribution License-
dc.subjectsynaptic transmission-
dc.subjectknock-out mice-
dc.subjectcalyx of Held-
dc.subjectcalcium currents-
dc.subjectP/Q channels-
dc.titleFunctional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal-
dc.typeJournal Article-
Appears in Collections:Published Articles, Dept. of Cell Physiology and Pharmacology

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