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C. Taki, T. Seki, M. Nakatani, Y. Shinohara, M. Ozawa, S. Nishimura, S. Shioda; Expression of the Receptor for Pituitary Adenylate Cyclase–Activating Polypeptide (PAC1–R) in the Retina With Kainic Acid–Induced Neurotoxicity . Invest. Ophthalmol. Vis. Sci. 2005;46(13):175.
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Purpose: The purpose of the present study was to examine the expression and localization of the PACAP receptor (PAC1–R) in the rat retina with kainic acid (KA)–induced neurotoxicity by immunohistochemistry. Methods: In the experiment group, 5 nmol of KA was injected into the vitreous of adult rat eyes. The eyes were enucleated and frozen sections of the posterior segments were prepared at 6 hours, 1 day, 2 days, 3 days and 7 days after KA injection. Immunohistochemistry was performed to examine the expression of PAC1–R in the retina. Double immunostaining of PAC1–R and glial fibrillary acidic protein (GFAP) was carried out to ascertain if PAC1–R immunoreactivity was localized in the glia. In addition, the excitotoxicity of KA was calculated by counting cells in the ganglion cell layer (GCL). Results: In untreated retinas, PAC1–R immunoreactivity was detected on the cell bodies in the GCL and inner nuclear layer (INL). PAC1–R positive cells in the INL were situated in the proximal region of this cell layer. At 6 hours to 1 day after injection of KA, increased immunoreactivity was observed on the cell bodies in the GCL and INL. At 2 days and subsequent time points, immunoreactivity of PAC1–R became detectable in the outer nuclear layer, nerve fiber layer (NFL) and inner limiting membrane (ILM). Immunoreactivity of GFAP, a reactive glial marker in the retina, was increasing with time after KA injection in the inner layer and in radial fibers throughout the retina. GFAP was colocalized with PAC1–R in the ILM. Morphometric analysis of retinal damage revealed a decrease in cell count in the GCL from 1 day after KA injection. Conclusions: KA injection caused a transient increase of PAC1–R immunoreactivity on the inner retinal neurons at early stages, when cell death in the GCL by KA was observed. Then delayed upregulation of PAC1–R occurred in the glia cells. Alterations in the expression of PAC1–R may be important in modulating neurotoxicity by KA.
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