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J. J. Pintor; Diadenosine Tetraphosphate Protects Sympathetic Terminals From 6-Hydroxydopamine Injury in the Ciliary Body. Invest. Ophthalmol. Vis. Sci. 2009;50(13):91.
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To investigate the role of the dinucleotide Ap4A in its ability to protect the ciliary body from neurodegeneration by 6-OHDA
Normotense New Zealand white rabbits (males, 2-3 kg) were used. All the nucleotides, dinucleotides and P2 antagonists were topically applied during 3 days before the application of 6-hydroxydopamine (6-OHDA) and 2 days after the treatment of 6-OHDA. Treatment with 6-hydroxydopamine (6-OHDA) was performed in 8 animals which the eyes were anesthetized with topical tetracaine and two injections of 0.1 ml of 10% 6-hydroxydopamine, freshly dissolved in 0.9% NaCl containing 0.5% ascorbic acid, in temporal and nasal regions was performed. Contralateral eyes were injected with 0.9% NaCl containing 0.5% ascorbic acid. IOP was measured by means of a Tonopen contact tonometer.
The application of 10 % 6-OHDA on normotense rabbits produces a dramatic decrease in IOP changing its values from 22.3 ± 1.4 mm Hg before the treatment, or in control animals, to 13.7 ± 1.2 mm Hg after the application of 6-OHDA. Pre-treatment of the animals with topical applications of the dinucleotide diadenosine tetraphosphate (Ap4A, 100 uM) for three days before 6-OHDA was applied and two days after, permitted to keep IOP in pressure values which were not statistically different from the ones in control animals (IOP value 21.9 ± 1.3 mm Hg). Immunohistochemical analysis of the sympathetic component that innervates the cilliary processes by means of VMAT2, permitted to see that in the presence of Ap4A (together with 6-OHDA) the sympathetic component remained intact in clear contrast with the treatment with 6-OHDA alone.
The application of the dinucleotide Ap4A protects the ciliary body sympathetic terminals from the destructive effect of 6-OHDA
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