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STEVEN G. KRAMER; Dopamine: A Retinal Neurotransmitter I. Retinal Uptake, Storage, and Light-Stimulated Release of H3-Dopamine in Vivo. Invest. Ophthalmol. Vis. Sci. 1971;10(6):438-452.
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Histochemical and chemical evidence has suggested the existence of dopaminergic neurons at the junction of the retinal inner nuclear and inner plexiform layers. In order that dopamine be identified as the chemical transmitter of these neurons, its uptake into the retina and release as a result of retinal stimulation must be shown. The present study revealed that uptake of H3-dopamine into the retina after carotid infusion was not inhibited by superior cervical ganglionectomy. In addition, exogenous dopamine was degraded to expected metabolites after uptake, and these were identified chromatographically. Subsequently, an experimental preparation in cats called preretinal perfusion was developed, and retinal uptake and light-stimulated release of tritiated dopamine was measured in vivo. The material released was chromatographically identified as dopamine. In dark-adapted animals, the rate of release and the amount of dopamine released per light flash increased nonlinearly with increasing flash frequency. In light-adapted animals, high rates of dopamine release were found regardless of flash frequency. On the basis of this and other evidence reviewed and to be presented in subsequent papers, it is suggested that dopamine acts as an inhibitory retinal neurotransmitter which may mediate a neural component of retinal sensitivity control.
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