Purchase this article with an account.
J. Vigh, C.W. Morgans, K. Rapp, E.M. Lasater; Characterization of the Voltage-gated Calcium Currents in Isolated Wide-field Amacrine Cells . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4137.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose:Calcium ions (Ca++) control processes in neurons as diverse as excitability, cell proliferation, neuronal development and transmitter release. Voltage-gated Ca++ channels are a major source of Ca++ in oscillating wide-field amacrine cells (WFACs) isolated from the teleost retina. Here we characterized the various, pharmacologically distinct Ca++ current (ICa) components in WFACs. Methods: Isolated cells from white bass retina were recorded from using standard whole-cell voltage clamp techniques. Membrane capacitance was monitored as the indicator of transmitter release following depolarizing voltage steps in the presence of TTX and cesium. Drugs were used at saturating concentrations. Results: Pharmacological investigation of the ICa in WFACs revealed at least three components. The largest portion (50-60%) was mediated by L-type channels, blocked by nifedipine or diltiazem, and enhanced by Bay-K. A smaller portion (about 30%) of the voltage-gated ICa enters the WFACs through Ω-conotoxin GVIA/MVIIC sensitive N-type channels. A mixture of diltiazem and GVIA and/or MVIIC never completely eliminated ICa; cobalt did. The ICa remaining after the mixture treatment contributes up to 20% of the total ICa in WFACs. Block of the L-type channels with diltiazem eliminated the membrane potential oscillations, but not GVIA. Diltiazem, Ω-conotoxin GVIA and SVIB as well as PLTX-II and sFTX 3.3 failed to block transmitter release from WFACs. Nevertheless, it was eliminated by cobalt or intracellular perfusion by 10 mM BAPTA. The spatial distribution of the pharmacologically distinct voltage-gated Ca++ channels was different. L-type channels were evenly distributed throughout the cell, but the N-type channels were found exclusively at the cell bodies and at the very proximal portions of the processes. WFACs never stained with R-type or P/Q-type antibodies. Conclusions: In WFACs the total ICa has at least three components: (1) L-type, mediating membrane potential oscillations; (2) N-type, possibly acting as a trigger for the oscillatoy membrane potentials in response to somatic excitatory (Glu) input, and (3) a drug resistant ICa component, likely to mediate transmitter release.
This PDF is available to Subscribers Only