June 2016
Volume 57, Issue 7
Open Access
Research Highlight  |   June 2016
Is Retinal Dopamine Involved in the Loss of Visual Function in Retinopathy of Prematurity?
Author Affiliations
  • P. Michael Iuvone
    Emory University Department of Ophthalmology, Atlanta, Georgia, United States; miuvone@emory.edu
Investigative Ophthalmology & Visual Science June 2016, Vol.57, 3380. doi:10.1167/iovs.16-20073
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      P. Michael Iuvone; Is Retinal Dopamine Involved in the Loss of Visual Function in Retinopathy of Prematurity?. Invest. Ophthalmol. Vis. Sci. 2016;57(7):3380. doi: 10.1167/iovs.16-20073.

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      © ARVO (1962-2015); The Authors (2016-present)

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Retinal dopamine, synthesized and released from dopamine amacrine cells (DACs), has been implicated in multiple aspects of visual function, including regulation of visual acuity and contrast sensitivity, light adaptation, circadian rhythms, and refractive development. Retinopathy of prematurity (ROP) is a devastating disease that can cause permanent loss of visual function, but the role of dopamine in this disorder is unclear. Oxygen-induced retinopathy (OIR) in laboratory animals has been used as an experimental model of ROP that recapitulates many of the features of the human disease. Oxygen-induced retinopathy and ROP occur in two distinct phases: a vaso-obliteration phase (I) and a neovascularization phase (II). Previous studies on dopamine in OIR have produced contradictory results, with one study reporting no change in the number of DACs1 and another study reporting a decrease in DAC processes and dopamine content.2 The paper of Spix and colleagues,3 published in this issue, greatly advances our knowledge of the changes to DACs during the progression of OIR in mice. They found no change in the number of DACs during phase I of OIR, but observed profound and irreversible loss of DACs and dopamine content in phase II. However, the DACs remaining after vasculature of the retina had returned to normal showed essentially normal electrophysiological properties, light responses, and dendritic morphology. These findings have important implications for the treatment of ROP if the results can be extrapolated to the human condition. They suggest that in order to preserve visual function, treatment for ROP must start early in the disease before the DACs die. Another interesting aspect of the relationship of OIR and dopamine pertains to refractive development. Oxygen-induced retinopathy is associated with myopic refractive errors, but through changes in the optical power of the anterior segment rather than through increased axial length.2 An unresolved question is whether retinal dopamine deficiency causes these changes in the anterior segment. 
References
Downie LE, Hatzopoulos KM, Pianta MJ, et al. Angiotensin type-1 receptor inhibition is neuroprotective to amacrine cells in a rat model of retinopathy of prematurity. J Comp Neurol. 2010; 518: 41–63.
Zhang N, Favazza TL, Baglieri AM, et al. The rat with oxygen-induced retinopathy is myopic with low retinal dopamine. Invest Ophthalmol Vis Sci. 2013; 54: 8275–8284.
Spix NJ, Liu L-L, Zhang Z, et al. Vulnerability of dopaminergic amacrine cells to chronic ischemia in a mouse model of oxygen-induced retinopathy. Invest Ophthalmol Vis Sci. 2016; 57: 3047–3057.
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