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Optometry & Vision Science:
doi: 10.1097/OPX.0000000000000208

Authors’ Response

Lan, Weizhong MD; Schaeffel, Frank PhD

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Tuebingen, Germany

We thank Drs. Norouzpour and Mehdizadeh for their interest in our study1 and appreciate their hypothesis that choroidal thickening might be driven by temperature elevation in the fundal layers, associated with bright light exposure. We have consulted the available literature and propose an experiment to confirm or refute their hypothesis.

Light absorption is one of the important functions of the retinal pigment epithelium (RPE). It was reported that light absorption by the melanosomes in the RPE could heat up the RPE/choroid complex.2 There appears to be a feedback-controlled regulation of temperature in the fundal layers, achieved by adjusting choroidal blood flow through choroidal vasodilation. It was shown to be modulated in both a passive3 and a reflexive manner.4,5 Nevertheless, if temperature elevation would be the primary reason for choroidal thickening in bright light, it should occur soon after the bright light was switched on. In our experiments, the increase in choroidal thickness was clearly delayed by hours or days.

A second question concerns the role of local temperature elevation in the control of retinal dopamine production and release. Although it is generally assumed that dopamine release is primarily controlled by light stimulating the photoreceptors, there is also evidence that tissue temperature plays a role. Brannan et al.6 reported a linear correlation between the dopamine release in the corpus striatum and core body temperature in anesthetized rats. Using electrophysiological approaches, Puopolo et al.7 found that response latencies and amplitudes in retinal dopaminergic neurons were also responsive to temperature changes, suggesting that the mechanism that delivers dopamine to the cell surface may also be temperature sensitive. Therefore, there is some evidence that temperature also controls dopamine release from the retina, in addition to light captured by the photoreceptors, and probably intrinsically photosensitive ganglion cells.8

Although the hypothesis proposed by Drs. Norouzpour and Mehdizadeh might not fully explain the mechanisms of (delayed) choroidal thickening in our study, or in other studies dealing with the role of choroidal thickness in myopia,9 it introduces an interesting question about the consequences of temperature elevation in the fundal layers. To differentiate effects caused by light captured by the photoreceptors from more unspecific effects of temperature elevation, invisible light could be used. Chicks could be kept under bright infrared light provided by high-power infrared light-emitting diodes. Energies should be matched to generate similar temperature elevation in the fundus. If increased dopamine release and associated inhibition of myopia would be observed, an interesting new approach could emerge to suppress myopia development by invisible light also in other species.

Weizhong Lan, MD

Frank Schaeffel, PhD

Tuebingen, Germany

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