Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
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 me...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2004 |
| País: | Argentina |
| Institución: | Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
| Repositorio: | Biblioteca Digital (UBA-FCEN) |
| Idioma: | inglés |
| OAI Identifier: | paperaa:paper_02706474_v24_n46_p10379_GonzalezInchauspe |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_02706474_v24_n46_p10379_GonzalezInchauspe |
| Access Level: | acceso abierto |
| Palabra clave: | Calcium currents Calyx of Held Facilitation Knock-out mice P/Q channels Synaptic transmission calcium channel N type calcium channel P type calcium channel Q type calcium ion animal tissue article calcium current channel gating facilitation knockout mouse mouse nerve cell plasticity nonhuman presynaptic membrane priority journal synaptosome transgenic mouse Animals Brain Stem Calcium Calcium Channels, N-Type Calcium Channels, P-Type Calcium Channels, Q-Type Evoked Potentials Mice Mice, Knockout Neuronal Plasticity Presynaptic Terminals Protein Subunits Synapses Synaptic Transmission |
| Sumario: | 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. |
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