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J. Troger, B. Teuchner, A. Amberger, J. Nemeth, E. Schmid, G. Kieselbach, M. Kralinger, N. Bechrakis; Vip, Pacap-38, Bdnf and Adnp in Nmda-Induced Excitotoxicity in the Rat Retina. Invest. Ophthalmol. Vis. Sci. 2009;50(13):89.
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© ARVO (1962-2015); The Authors (2016-present)
To determine whether retinal BDNF, VIP, PACAP-38 and ADNP are affected following an intravitreal injection of NMDA into the rat eye and to investigate whether flunarizine nullifies these effects.
2 microliters of 100nmol NMDA was injected into the vitreous of one rat eye and vehicle into the other eye. Both eyes of animals were topically treated with 2% flunarizine twice daily or only vehicle. Animals were sacrificed after defined times and the retina analysed for PACAP-38, VIP and BDNF proteins using radioimmunoassay and ELISA, respectively. The expression of mADNP was determined by quantitative RT-PCR.
In contrast to PACAP-38, VIP levels had significantly decreased on days 1, 7, 14, 28 and 56 after NMDA injection and flunarizine not only reversed this effect but also increased the levels per se. BDNF levels had significantly increased after days one and three and the expression of ADNP had decreased in the treated retina.
In contrast to PACAP-38 containing ganglion and amacrine cells, VIP-ergic amacrine cells are susceptible to NMDA-excitotoxicity, indicating that certain amacrine cells are more vulnerable than at least PACAP-expressing cells and furthermore, flunarizine acts neuroprotectively. Since both VIP, PACAP-38, BDNF and ADNP feature neuroprotective effects in vitro and/or in vivo in the retina they may well be integrated in endogenous neuroprotective mechanisms which break down in NMDA excitotoxicity. The maintenance, preservation and support of these mechanisms must be the primary aim in the therapy of diseases such as glaucoma and this constitutes a novel and alternative approach.
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