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Retinal Degeneration in the nervous Mutant Mouse. IV. Inner Retinal Changes

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Abstract

We have recently noted that the inner nuclear layer (INL) and the inner plexiform layer (IPL) were significantly thinner in mice homozygous for the nervous defect (nr / nr) than in control (nr /+ or +/+) littermates. Here, we have carried out a series of anatomical studies to further understand these inner retinal changes. At postnatal day (P) 13, there was no difference in the inner retina between nervous and control mice, while a significant difference was observed at P30. Similar changes were not seen in other mouse models of photoreceptor degeneration. There was a significant reduction in the density of cells in the INL that were stained by antibodies against the inhibitory neurotransmitters GABA and glycine. These results indicate that the nervous defect causes a degeneration of one or more sub-types of amacrine cells, in addition to the loss of cerebellar Purkinje cells and retinal photoreceptors that is known to occur in these mutant animals. Finally, evidence is provided that photoreceptors die by an apoptotic pathway in nervous mice.

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    f2

    Current address: Department of Cell Biology, Oklahoma University Health Science Center, Oklahoma City, OK 73104, U.S.A.

    f1

    Address correspondence to: Neal S. Peachey, Cole Eye Institute (i -31), Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, U.S.A. E.-mail: [email protected]

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