Ionic Mechanisms Mediating Oscillatory Membrane Potentials in Wide-Field Retinal Amacrine Cells

• Published in: Journal of neurophysiology 2003-07, Vol.90 (1), p.431-443
• Main Authors: Vigh, Jozsef, Solessio, Eduardo, Morgans, Catherine W, Lasater, Eric M
• Format: Article
• Language: English
• Subjects: Amacrine Cells - drug effects; Amacrine Cells - physiology; Animals; Bass; Calcium Channel Blockers - pharmacology; Calcium Channels - metabolism; Calcium Channels - physiology; Calcium Signaling; Fluorescent Antibody Technique; Membrane Potentials; Patch-Clamp Techniques; Periodicity; Potassium Channel Blockers - pharmacology; Potassium Channels - metabolism; Retina - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.00092.2003

1 Department of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah, Health Sciences Center, Salt Lake City, Utah 84132; 2 Department of General Zoology and Neurobiology, University of Pécs, Faculty of Natural Sciences, Pécs, H-7601 Hungary; 3 Center for Vision Research, State University of New York, Upstate Medical University, Syracuse, New York 13210; and 4 Neurological 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 (Ca 2 + ) dependent; blocking voltage-gated Ca 2 + channels eliminated the oscillations, whereas elevating extracellular Ca 2 + enhanced them. Strong intracellular Ca 2 + buffering (10 mM EGTA or bis-( o -aminophenoxy)- N,N,N ' ,N '-tetraacetic acid) eliminated any attenuation in the OMPs as well as a Ca 2 + -dependent inactivation of the voltage-gated Ca 2 + channels. Pharmacological and immunohistochemical characterization revealed that WFACs express L- and N-type voltage-sensitive Ca 2 + 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 Ca 2 + 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 Ca 2 + channel. Address for reprint requests: E. M. Lasater, Dept. of Ophthalmology and Visual Sciences, John Moran Eye Center, University of Utah, 50 N. Medical Dr., Salt La