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R.E. Rosenstein, A.P. Goldin, E. Salido, M. Chianelli, M.I. Keller Sarmiento, D.A. Sáenz; Effect of Melatonin on the Glutamate/Glutamine Cycle Activity in the Golden Hamster Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4005.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Glutamate is the main excitatory neurotransmitter in the retina but it is neurotoxic when present in excessive amounts. Retinal glutamate synaptic concentrations are regulated by the activity of the glutamate/glutamine cycle. Since melatonin has been shown to be neuroprotective in several systems, in the present report, its effect on the glutamate/glutamine cycle activity was examined in the golden hamster retina Methods: Glutamine synthetase (GS) activity was assessed by a spectrophotometric assay, whereas glutamine uptake and release were assessed using [3H]–glutamine as a radioligand. In addition, glutaminase activity was measured through the conversion of [3H]–glutamine to [3H]–glutamate. Results: Melatonin (0.1 – 10 nM) significantly increased retinal glutamine synthetase activity but it did not affect L–glutamine release. A characterization of the hamster retinal L–glutamine uptake mechanism was performed. This mechanism was partly Na+–dependent, and it was significantly inhibited by 2–aminobicyclo (2,2,1) heptane 2–carboxylic acid (BCH, a selective antagonists for the L–type system) and by α–(methylamino)–isobutyric acid (MeAIB, substrate characteristic for the A –type transporter) suggesting the coexistence of these transport systems in the hamster retina. Melatonin (0.1 – 10 nM) significantly increased total glutamine uptake as well as the BCH and the MeAIB –insensitive transporters activity. On the other hand, melatonin significantly decreased retinal glutaminase activity. Conclusions: Based on these results, it might be presumed that hamster retinal glutamate /glutamine cycle activity is regulated by physiological concentrations of melatonin. Furthermore, these findings suggest that a treatment with melatonin could be considered as a new approach to handling glutamate–mediated neuronal degeneration.
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