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1Department of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah, Health Sciences Center, Salt Lake City, Utah 84132; 2Department of General Zoology and Neurobiology, University of Pécs, Faculty of Natural Sciences, Pécs, H-7601 Hungary; 3Center for Vision Research, State University of New York, Upstate Medical University, Syracuse, New York 13210; and 4Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006
Submitted 30 January 2003; accepted in final form 2 March 2003
Particular types of amacrine cells of the vertebrate retina show
oscillatory membrane potentials (OMPs) in response to light stimulation.
Historically it has been thought the oscillations arose as a result of circuit
properties. In a previous study we found that in some amacrine cells, the
ability to oscillate was an intrinsic property of the cell. Here we
characterized the ionic mechanisms responsible for the oscillations in
wide-field amacrine cells (WFACs) in an effort to better understand the
functional properties of the cell. The OMPs were found to be calcium
(Ca2+) dependent; blocking voltage-gated
Ca2+ channels eliminated the oscillations, whereas
elevating extracellular Ca2+ enhanced them. Strong
intracellular Ca2+ buffering (10 mM EGTA or
bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic
acid) eliminated any attenuation in the OMPs as well as a
Ca2+-dependent inactivation of the voltage-gated
Ca2+ channels. Pharmacological and immunohistochemical
characterization revealed that WFACs express L- and N-type voltage-sensitive
Ca2+ channels. Block of the L-type channels eliminated
the OMPs, but 
-conotoxin GVIA did not, suggesting a different function
for the N-type channels. The L-type channels in WFACs are functionally coupled
to a set of calcium-dependent potassium (K(Ca)) channels
to mediate OMPs. The initiation of OMPs depended on penitrem-A-sensitive (BK)
K(Ca) channels, whereas their duration is under
apamin-sensitive (SK) K(Ca) channel control. The
Ca2+ current is essential to evoke the OMPs and
triggering the K(Ca) currents, which here act as resonant
currents, enhances the resonance as an amplifying current, influences the
filtering characteristics of the cell membrane, and attenuates the OMPs via
CDI of the L-type Ca2+ channel.
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