10379.full.pdf (221.13 kB)
Download file

Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal

Download (221.13 kB)
journal contribution
posted on 24.10.2012, 09:00 by C. González Inchauspe, F. J. Martini, O. D. Uchitel, Ian D. Forsythe
Calcium 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.

Funding

This 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

History

Citation

Journal of Neuroscience, 2004, 24 (46), pp. 10379-10383

Published in

Journal of Neuroscience

Publisher

Society for Neuroscience

issn

0270-6474

eissn

1529-2401

Available date

24/10/2012

Publisher version

http://www.jneurosci.org/content/24/46/10379

Language

en