Abstract
Abstract: :
Purpose: To evaluate the phenotypic expression of AII amacrine cell in the axotomy rat retina using immunocytochemistry with antisera against parvalbumin and disabled–1. Methods: We performed the double labeling immunohistochemistry in vibratome section (50 um) of axotomy rat retina. For double–label studies, sections were incubated overnight in a mixture of anti–parvalbumin antibody (1:500; Sigma) with the following antibodies: polyclonal anti–glycine (1:8000; kindly provided by Dr. D. Pow, University of Queensland), polyclonal anti–connexin 36 (Cx36) antibody (1:1000; Zymed Laboratories) and polyclonal anti–Dab1 (1:1000). For BDNF injection, human recombinant BDNF (5 µg in 5 µl sterile saline; Regeneron Pharmaceuticals, Tarrytown, NY, USA) was injected into the vitreal chamber of each eye immediately after the optic nerve transection, using a Hamilton syringe with a 30–gauge needle. Results: Parvalbumin immunoreactivity was present in cell bodies and processes of AII amacrine cell bodies at control retina and retina at 7 days after optic nerve transcetion (ONT). However, in the retina at 14 days after ONT, parvalbumin immunoreactivity was only present in cell bodies and few lobular apendages. There was no changes of connexin 36 immunoreactivties during experimental periods. Double–labeling experiments using antisera against parvalbumin and Dab1 demonstrated that parvalbumin immunoreactivity was shift to cell bodies of AII amacrine cells and a few bipolar cells at 14 days after ONT. After BDNF treatment, parvalbumin immunoreactivity appeared again in whole processes of AII amacrine cells at 14 days after ONT. Conclusions: These findings indicate that BDNF is essential for maintenance of normal functions of AII amacrine cells.
Keywords: amacrine cells • retina: proximal (bipolar, amacrine, and ganglion cells) • retina