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The effects of nicotine on cone and rod b-wave responses in larval zebrafish

Published online by Cambridge University Press:  28 June 2013

MIGUEL MOYANO
Affiliation:
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts Instituto de Neurosciencias of Castilla y Leon, Cell Biology and Pathology, University of Salamanca, Salamanca, Spain
ÁNGEL PORTEROS
Affiliation:
Instituto de Neurosciencias of Castilla y Leon, Cell Biology and Pathology, University of Salamanca, Salamanca, Spain
JOHN E. DOWLING*
Affiliation:
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts
*
*Address correspondence to: John E. Dowling, Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, E-mail: dowling@mcb.harvard.edu

Abstract

Acetylcholine is present in and released from starburst amacrine cells in the inner plexiform layer (IPL), but its role in retinal function except, perhaps, in early development, is unclear. Nicotinic acetylcholine receptors are thought to be present on ganglion, amacrine, and bipolar cell processes in the IPL, and it is known that acetylcholine increases the spontaneous and light-evoked responses of retinal ganglion cells. The effects of acetylcholine on bipolar cells are not known, and here we report the effects of nicotine on the b-wave of the electroretinogram in larval zebrafish. The b-wave originates mainly from ON-bipolar cells, and the larval zebrafish retina is cone-dominated. Only small rod responses can be elicited with dim lights in wild-type larval zebrafish retinas, but rod responses can be recorded over a range of intensities in a mutant (no optokinetic response f) fish that has no cone function. We find that nicotine strongly enhances cone-driven b-wave response amplitudes but depresses rod driven b-wave response amplitudes without, however, affecting rod- or cone-driven b-wave light sensitivity.

Type
Research Articles
Copyright
Copyright © Cambridge University Press 2013 

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