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Hiroshi Ohguro, Kei-ichi Ogawa, Tadao Maeda, Ikuyo Maruyama, Akiko Maeda, Yoshiko Takano, Mitsuru Nakazawa; Retinal Dysfunction in Cancer-Associated Retinopathy Is Improved by Ca2+ Antagonist Administration and Dark Adaptation. Invest. Ophthalmol. Vis. Sci. 2001;42(11):2589-2595.
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purpose. It was recently found that recoverin acts as an autoantigen recognized
by sera of patients with cancer-associated retinopathy (CAR), and that
CAR-like retinal dysfunction is produced by intravitreous
administration of anti-recoverin antibody in Lewis rat eyes. To examine
the pathologic molecular mechanism of CAR, and to elucidate an
effective therapy for CAR, the function and morphology of CAR were
compared with those of phototoxic retinal damage, another form of
photoreceptor dysfunction, and the effect of nilvadipine, a
Ca2+ antagonist, on the retinal degenerations was studied,
using these models.
methods. Under different illumination conditions and/or medication with
nilvadipine, the functional and morphologic properties of the
retinas were evaluated after intravitreous injection of anti-recoverin
antibody into Lewis rat eyes (six rats, 12 eyes in each experimental
condition), using electroretinogram (ERG), rhodopsin phosphorylation,
and light microscopy.
results. Anti-recoverin antibody administered into the vitreous of Lewis rat
eyes induced a significant decrease and increase of ERG responses and
rhodopsin phosphorylation levels, respectively, under cyclic or
continuous light. Similar changes were observed in eyes of rats bred
under continuous illumination that did not receive anti-recoverin
antibodies. However, anti-recoverin antibody–induced retinal
dysfunctions were not observed in rat eyes under dark conditions.
Administration of nilvadipine, a Ca2+ antagonist, to the
anti-recoverin antibody–treated rats and rats with phototoxic retinal
dysfunction caused significant improvement of the deterioration of ERG
and normalization of rhodopsin phosphorylation.
conclusions. The present data indicate that anti-recoverin antibody–induced retinal
dysfunction was functionally similar to phototoxic retinal dysfunction
and was markedly suppressed under dark conditions or by systemic
administration of a Ca2+ antagonist.
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