Journal
JOURNAL OF NEUROSCIENCE
Volume 32, Issue 27, Pages 9359-9368Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0711-12.2012
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Funding
- National Institutes of Health [R01EY15815, T32EY07135, P30EY008126, R01EY004864, P30EY006360, R01MH086629, T32EY07092]
- Katz Foundation
- Research to Prevent Blindness (RPB), New York
- Senior Scientific Investigator Award from RPB
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Dopamine is a key neuromodulator in the retina and brain that supports motor, cognitive, and visual function. Here, we developed a mouse model on a C57 background in which expression of the rate-limiting enzyme for dopamine synthesis, tyrosine hydroxylase, is specifically disrupted in the retina. This model enabled assessment of the overall role of retinal dopamine in vision using electrophysiological (electroretinogram), psychophysical (optokinetic tracking), and pharmacological techniques. Significant disruptions were observed in high-resolution, light-adapted vision caused by specific deficits in light responses, contrast sensitivity, acuity, and circadian rhythms in this retinal dopamine-depleted mouse model. These global effects of retinal dopamine on vision are driven by the differential actions of dopamine D1 and D4 receptors on specific retinal functions and appear to be due to the ongoing bioavailability of dopamine rather than developmental effects. Together, our data indicate that dopamine is necessary for the circadian nature of light-adapted vision as well as optimal contrast detection and acuity.
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