Author:
VIGH JOZSEF,LASATER ERIC M.
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).
Publisher
Cambridge University Press (CUP)
Subject
Sensory Systems,Physiology
Cited by
21 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献