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L-type calcium channels mediate transmitter release in isolated, wide-field retinal amacrine cells

Published online by Cambridge University Press:  23 June 2004

JOZSEF VIGH
Affiliation:
Department of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah, Health Sciences Center, Salt Lake City Department of General Zoology and Neurobiology, University of Pecs, Pecs, H-7624 Hungary Present address of J. Vigh: Vollum Institute, Oregon Health and Sciences University, Portland, OR 97201, USA.
ERIC M. LASATER
Affiliation:
Department of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah, Health Sciences Center, Salt Lake City

Abstract

Transmitter release in neurons is triggered by intracellular Ca2+ increase via the opening of voltage-gated Ca2+ channels. Here we investigated the voltage-gated Ca2+ channels in wide-field amacrine cells (WFACs) isolated from the white-bass retina that are functionally coupled to transmitter release. We monitored transmitter release through the measurement of the membrane capacitance (Cm). We found that 500-ms long depolarizations of WFACs from −70 mV to 0 mV elicited about a 6% transient increase in the Cm or membrane surface area. This Cm jump could be eliminated either by intracellular perfusion with 10 mM BAPTA or by extracellular application of 4 mM cobalt. WFACs possess N-type and L-type voltage-gated Ca2+ channels. Depolarization-evoked Cm increases were unaffected by the specific N-type channel blocker ω-conotoxin GVIA, but they were markedly reduced by the L-type blocker diltiazem, suggesting a role for the L-type channel in synaptic transmission. Further supporting this notion, in WFACs the synaptic protein syntaxin always colocalized with the pore-forming subunit of the retinal specific L-type channels (CaV1.4 or α1F), but never with that of the N-type channels (CaV2.2 or α1B).

Type
Research Article
Copyright
2004 Cambridge University Press

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