Hostname: page-component-848d4c4894-tn8tq Total loading time: 0 Render date: 2024-06-20T16:40:47.767Z Has data issue: false hasContentIssue false
  • English
  • Français

Tunicamycin-induced degeneration in cone photoreceptors

Published online by Cambridge University Press:  02 June 2009

Don H. Anderson ,
David S. Williams ,
Jay Neitz ,
Robert N. Fariss  and
Steven J. Fliesler
Don H. Anderson
Affiliation:
IES, Neuroscience Research Program, University of California, Santa Barbara
David S. Williams
Affiliation:
Department of Visual Science, School of Optometry, Indiana University, Bloomington
Jay Neitz
Affiliation:
Department of Psychology, University of California, Santa Barbara
Robert N. Fariss
Affiliation:
IES, Neuroscience Research Program, University of California, Santa Barbara
Steven J. Fliesler
Affiliation:
Bethesda Eye Institute and Department of Biochemistry, St. Louis School of Medicine, St. Louis
Get access Rights & Permissions [Opens in a new window]

Abstract

Tunicamycin (TM), an inhibitor of dolichylphosphate-mediated protein glycosylation, was injected intravitreally into the eyes of diurnal rodents with cone-dominated retinas. Injection of 1 μg of the B2 isomer led to a progressive degeneration of the photoreceptor outer segments and disruption of the RPE-photoreceptor interface that took place over a 10-day period. Cone outer segments were shortened by postinjection day 6 and virtually absent by day 9. The microvilli that normally protrude from the apical surface of the retinal pigment epithelium were replaced by a fringe of shortened processes. The other retinal layers showed no morphological evidence of disruption. Retinal sensitivity, as measured by electroretinographic b-wave threshold, showed a significant and progressive decline over the 10-day course of the experiment that paralleled the disruption of retinal morphology. These results suggest that TM leads to similar morphological and electrophysiological effects on rod and cone photoreceptors.

Keywords

TunicamycinPhotoreceptorsRetinaDegeneration
Type
Research Article
Information
Visual Neuroscience , Volume 1 , Issue 2 , March 1988 , pp. 153 - 158
Copyright
Copyright © Cambridge University Press 1988

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Defoe, D.M., Besharse, J.C. & Fliesler, S.J. (1986). Tunicamycin-induced dysgenesis of retinal rod outer segment membranes. II. Quantitative freeze-fracture analysis. Investigative Ophthalmology and Visual Science 27, 1595–1602.Google ScholarPubMed
Duksin, D. & Mahoney, W.C. (1982). Relationship of the structure and biological activity of the natural homologues of tunicamycin. Journal of Biological Chemistry 257, 3105–3109.CrossRefGoogle ScholarPubMed
Elbein, A.D. (1984). Inhibitors of the biosynthesis and processing of N-linked oligosaccharides. CRC Critical Reviews of Biochemistry 16, 21–49.CrossRefGoogle ScholarPubMed
Fliesler, S.J. & Basinger, S.F. (1985). Tunicamycin blocks the incorporation of opsin into retinal rod outer segment membranes. Proceedings of the National Academy of Science (USA) 82, 1116–1120.CrossRefGoogle ScholarPubMed
Fliesler, S.J., Rapp, L.M., & Hollyfield, J.G. (1984a). Photoreceptor-specific degeneration caused by tunicamycin. Nature (Lond) 311, 575–577.CrossRefGoogle ScholarPubMed
Fliesler, S.J., Rapp, L.M., Rayborn, M.E., & Hollyfield, J.G. (1985b). Defects in retinal glycoprotein metabolism: putative role in photoreceptor degenerations. In Retinal Degeneration: Contemporary Experimental and Clinical Studies, ed. Lavail, M.M., Hollyfield, J.G., & Anderson, R.E., pp. 349–371. New York: A.R. Liss, Inc.Google Scholar
Fliesler, S.J., Rayborn, M.E., & Hollyfield, J.G. (1985a). Membrane morphogenesis in retinal rod outer segments: inhibition by tunicamycin. Journal of Cell Biology 100, 574–587.CrossRefGoogle ScholarPubMed
Fliesler, S.J., Rayborn, M.E., & Hollyfield, J.G. (1986). Protein-bound carbohydrate involvement in plasma membrane assembly: the retinal rod photoreceptor cell as a model. In Protein-Carbohydrate Interactions in Biological Systems, ed. Lark, D.L., pp. 191–205. London: Academic Press.Google Scholar
Fliesler, S.J., Tabor, G.A., & Hollyfield, J.G. (1984b). Glycoprotein synthesis in the human retina: localization of the lipid intermediate pathway. Experimental Eye Research 39, 153–173.CrossRefGoogle ScholarPubMed
Garcia, C.A., Chu, H.H., Matheny, J.L., Chu, L., Zhuang, S., Venger, C., & Fliesler, S.J. (1985). Tuncamycin-induced retinal degeneration in rabbit and primate retinas. Investigative Ophthalmology and Visual Science (ARVO suppl.) 26, 34.Google Scholar
Long, K.O. & Fisher, S.K. (1983). Spermophilus beecheyi. Journal of Comparative Neutrology 221, 329–340.CrossRefGoogle ScholarPubMed
Long, K.O., Fisher, S.K., Fariss, R.N., & Anderson, D.H. (1986). Disc shedding and autophagy in the cone-dominant ground squirrel retina. Experimental Eye Research 43, 193–205.CrossRefGoogle ScholarPubMed
Plantner, J.J., Poncz, L. & Kean, E.L. (1980). Effect of tunicamycin on glycosylation of rhodopsin. Archives of Biochemistry and Biophysics 201, 527–532.CrossRefGoogle ScholarPubMed
Schwarz, R.T. & Datema, R. (1982). The lipid intermediate pathway of protein glycosylation and its inhibitors; the biological significance of protein-bound carbohydrates. Advances in Carbohydrate Chemistry and Biochemistry 40, 287–379.CrossRefGoogle Scholar
Ulshafer, R.J., Allen, C.B. & Fliesler, S.J. (1986). Tunicamycin-induced dysgenesis of retinal rod outer segment membranes. I. A scanning electron microscopy study. Investigative Ophthalmology and Visual Science 27, 1587–1594.Google Scholar