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Retinal degeneration during clinical scrapie encephalopathy in hamsters
Author(s) -
Buyukmihci Ned,
GoehringHarmon Faye,
Marsh Richard F.
Publication year - 1982
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902050206
Subject(s) - scrapie , biology , retina , retinal pigment epithelium , retinal , retinal degeneration , inner plexiform layer , pathology , outer plexiform layer , degeneration (medical) , encephalopathy , anatomy , neuroscience , medicine , prion protein , biochemistry , disease
Weanling hamsters were inoculated intracerebrally with brain suspensions from normal or scrapie‐infected hamsters. A third group of uninoculated animals was fed cuprizone. Histologic and electron microscopic examination of the neural retinas and retinal pigment epithelium was done. At 50 days postinoculation, when scrapie‐infected animals began to show clinical signs of encephalopathy, there was a variable degree of photoreceptor degeneration. By the time animals were moribund, at 74 days postinoculation, photoreceptor degeneration was severe, as demonstrated by loss of most outer and inner segments and cell bodies. The outer plexiform, inner nuclear, and inner plexiform layers were reduced in thickness. Some retinal pigment epithelial cells contained lipoidal inclusions. The neural retinas and retinal pigment epithelium of noninfected and cuprizone‐treated animals were normal. We have previously shown that the scrapie agent accumulates in the retina; that together with our present work, we conclude that the scrapie agent is the cause of photoreceptor degeneration in experimentally inoculated hamsters.