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L-type calcium channels mediate transmitter release in isolated, wide-field retinal amacrine cells
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 releas...
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Published in: | Visual neuroscience 2004-03, Vol.21 (2), p.129-134 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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). |
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ISSN: | 0952-5238 1469-8714 |
DOI: | 10.1017/S095252380404204X |