Light-Evoked Responses of Bipolar Cells in a Mammalian Retina

Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, Massachussetts 02114 Euler, Thomas and Richard H. Masland. Light-Evoked Responses of Bipolar Cells in a Mammalian Retina. J. Neurophysiol. 83: 1817-1829, 2000. We recorded light-evoked responses from rod and cone bipolar cells...

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Veröffentlicht in:Journal of neurophysiology 2000-04, Vol.83 (4), p.1817-1829
Hauptverfasser: Euler, Thomas, Masland, Richard H
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Sprache:eng
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Zusammenfassung:Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, Massachussetts 02114 Euler, Thomas and Richard H. Masland. Light-Evoked Responses of Bipolar Cells in a Mammalian Retina. J. Neurophysiol. 83: 1817-1829, 2000. We recorded light-evoked responses from rod and cone bipolar cells using patch-clamp techniques in a slice preparation of the rat retina. Rod bipolar cells responded to light with a sustained depolarization ( ON response) followed at light offset by a slight hyperpolarization. ON and OFF cone bipolar cells were encountered, both with diverse temporal properties. The responses of rod bipolar cells were composed primarily of two components, a nonspecific cation current and a chloride current. The chloride current was reduced greatly in axotomized cells and could be suppressed by coapplication of the GABA A antagonist bicuculline and the GABA C antagonist (1,2,5,6-tetrahydropyridine-4-yl)methylphosphinic acid. This suggests that it largely reflects feedback from GABAergic amacrine cells. The response latency of intact rod bipolar cells was shorter than that of the axotomized cells, and the sensitivity curve covered more than twice the dynamic range. Application of the GABA receptor antagonists partially mimicked the effects of axotomy. These findings suggest that functional properties of the axon terminal system notably synaptic feedback from amacrine cells play an important role in defining the response properties of mammalian bipolar cells.
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.2000.83.4.1817