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(Investigative Ophthalmology and Visual Science. 2000;41:3128-3133.)
© 2000 by The Association for Research in Vision and Ophthalmology, Inc.

Retinal Dysfunction in Basigin Deficiency

Kenji Hori1, Naomi Katayama4, Shu Kachi1,2, Mineo Kondo1, Kenji Kadomatsu3, Jiro Usukura2, Takashi Muramatsu3, Shigeo Mori4 and Yozo Miyake1

From the 1 Departments of Ophthalmology, 2 Anatomy, and 3 Biochemistry, Nagoya University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya, Japan; and 4 Space Medicine Research Center, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

PURPOSE. To examine the retina of basigin (Bsg) knockout mice by electrophysiological and histologic methods and thereby to determine the possible function of Bsg in phototransduction and retinal development.

METHODS. Scotopic and photopic electroretinograms (ERGs) were recorded from 11 wild-type, 12 heterozygous, and 8 homozygous Bsg gene knockout mice of different ages. The retinas were also examined by histologic and immunolabeling methods.

RESULTS. Bsg knockout mice of 5 to 41 weeks of age showed a decrease in the amplitude of all components of both the photopic and scotopic ERGs. In contrast, the fundus and the fluorescein fundus angiography and morphology of the retina at the light microscopic level appeared to be normal until 8 weeks of age in Bsg knockout mice. Thereafter, the length of outer segment and outer nuclear layers decreased with increasing age. Immunohistochemical analysis localized Bsg protein in a variety of cells in the retina, especially in the pigment epithelium, the upper outer plexiform layer and the inner segments of photoreceptor cells.

CONCLUSIONS. The results demonstrated that both rod and cone function were severely affected from an early age by the targeted disruption of the Bsg gene. In spite of abnormal ERGs, the photoreceptor cells maintained normal morphology up to 8 weeks. Thereafter, the photoreceptor cells degenerated gradually and were almost ablated by 41 weeks.




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