LIGHT-INDUCED-CHANGES IN S-ANTIGEN (ARRESTIN) LOCALIZATION IN RETINALPHOTORECEPTORS - DIFFERENCES BETWEEN RODS AND CONES AND DEFECTIVE PROCESS IN RCS RAT RETINAL DYSTROPHY

Citation
M. Mirshahi et al., LIGHT-INDUCED-CHANGES IN S-ANTIGEN (ARRESTIN) LOCALIZATION IN RETINALPHOTORECEPTORS - DIFFERENCES BETWEEN RODS AND CONES AND DEFECTIVE PROCESS IN RCS RAT RETINAL DYSTROPHY, European journal of cell biology, 63(1), 1994, pp. 61-67
Citations number
40
Categorie Soggetti
Cytology & Histology
ISSN journal
01719335
Volume
63
Issue
1
Year of publication
1994
Pages
61 - 67
Database
ISI
SICI code
0171-9335(1994)63:1<61:LIS(LI>2.0.ZU;2-8
Abstract
The subcellular localization of S-antigen (arrestin), a protein regula ting phototransduction in retinal rods, was studied by immuno-cytochem istry using monoclonal antibodies on sections of Swiss mouse, Lewis, B rown Norway (BN), Royal College of Surgeons (RCS) rdy-p(+) (dystrophic ) and RCS rdy(+)-p (non-dystrophic) rat retinas. In normal retinas, th e topography of S-antigen immuno-reactivity in photoreceptor cells var ied according to the lighting environment of the animals. In dark-adap ted eyes, outer segments did not display any S-antigen immunoreactivit y while the inner segments, cell bodies and synaptic terminals were st rongly labeled. A few minutes after light exposure, there was an inver sion of the pattern of labeling: the label increased in the outer segm ent but was strongly reduced in the other compartments. After Ih of li ght, S-antigen immunoreactivity remained only in outer segments and in a few synaptic terminals. We show that the kinetics of this change is slower in cone than in rod cells, and thus allows the transient visua lization of the scarce cone photoreceptors. On the 17th day after birt h, photoreceptor cells are well differentiated in all rat strains, inc luding RCS rdy-p(+) rats. At this time, the S-antigen shift phenomenon occurred in the non-dystrophic strains, but was not observed in rdy-p (+) rats: after light exposure, the intracellular distribution of S-an tigen remained the same as in the dark. We suggest that an abnormality in the mechanisms of intracellular protein transport could be a chara cteristic of this genetic disease.