The first two authors contributed equally to this work.
Dopamine and full-field illumination activate D1 and D2-D5-type receptors in adult rat retinal ganglion cells
Article first published online: 1 OCT 2012
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Comparative Neurology
Volume 520, Issue 17, pages 4032–4049, 1 December 2012
How to Cite
Ogata, G., Stradleigh, T. W., Partida, G. J. and Ishida, A. T. (2012), Dopamine and full-field illumination activate D1 and D2-D5-type receptors in adult rat retinal ganglion cells. J. Comp. Neurol., 520: 4032–4049. doi: 10.1002/cne.23159
- Issue published online: 1 OCT 2012
- Article first published online: 1 OCT 2012
- Accepted manuscript online: 8 JUN 2012 01:43AM EST
- Manuscript Accepted: 1 JUN 2012
- Manuscript Revised: 14 MAY 2012
- Manuscript Received: 19 APR 2012
- National Institutes of Health (NIH). Grant Number: EY08120
- NIH American Recovery and Reinvestment Act Award. Grant Number: EY08120-20S1
- National Eye Institute Core grant. Grant Number: P30 EY12576
- Department of Ophthalmology from Research to Prevent Blindness, Inc., New York, NY departmental grant
- NIH-IMSD Fellowship. Grant Number: R25 56765
- NIH-NEI Training Grant. Grant Number: T32 EY015387
- NIH Research Supplement to Promote Diversity in Health-Related Research. Grant Number: EY08120-17S1
Dopamine can regulate signal generation and transmission by activating multiple receptors and signaling cascades, especially in striatum, hippocampus, and cerebral cortex. Dopamine modulates an even larger variety of cellular properties in retina, yet has been reported to do so by only D1 receptor-driven cyclic adenosine monophosphate (cAMP) increases or D2 receptor-driven cAMP decreases. Here, we test the possibility that dopamine operates differently on retinal ganglion cells, because the ganglion cell layer binds D1 and D2 receptor ligands, and displays changes in signaling components other than cAMP under illumination that should release dopamine. In adult rat retinal ganglion cells, based on patch-clamp recordings, Ca2+ imaging, and immunohistochemistry, we find that 1) spike firing is inhibited by dopamine and SKF 83959 (an agonist that does not activate homomeric D1 receptors or alter cAMP levels in other systems); 2) D1 and D2 receptor antagonists (SCH 23390, eticlopride, raclopride) counteract these effects; 3) these antagonists also block light-induced rises in cAMP, light-induced activation of Ca2+/calmodulin-dependent protein kinase II, and dopamine-induced Ca2+ influx; and 4) the Ca2+ rise is markedly reduced by removing extracellular Ca2+ and by an IP3 receptor antagonist (2-APB). These results provide the first evidence that dopamine activates a receptor in adult mammalian retinal neurons that is distinct from classical D1 and D2 receptors, and that dopamine can activate mechanisms in addition to cAMP and cAMP-dependent protein kinase to modulate retinal ganglion cell excitability. J. Comp. Neurol. 520:4032–4049, 2012. © 2012 Wiley Periodicals, Inc.