Retinal degeneration in the mouse. A model induced transplaceatally by methylnitrosourea

Sylvia B Smith, K. Lemone Yielding

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

A model of retinal degeneration has been developed in mice which is induced by the DNA alkylating agent methylnitrosourea. Pregnant mice were injected with various doses of this potent teratogen on day 16 of gestation, a time of differentiation of numerous cell types of the mouse retina. Histological examination of retinas from offspring exposed to 20-, 10- and 5 mg kg-1 doses demonstrated retinal rosettes, a pathology similar to retinal dysplasia. The 1 mg kg-1 dosage did not produce rosettes; in fact, retinas appeared morphologically normal early in life. Control and treated animals were studied at specific age intervals: 2-, 4-, 6-, 8-, 12-, 16-, 20-, 36-, 52 weeks. Measurements of the overall retinal width and five retinal layers were made to quantify the degeneration. Results indicate a thinning of the retina begins at 4 weeks and worsens with age. These results are discussed with respect to the potential of low-level exposure to environmental toxins as a possible cause of retinal degeneration.

Original languageEnglish (US)
Pages (from-to)791-801
Number of pages11
JournalExperimental Eye Research
Volume43
Issue number5
DOIs
StatePublished - Jan 1 1986
Externally publishedYes

Fingerprint

Methylnitrosourea
Retinal Degeneration
Retina
Retinal Dysplasia
Teratogens
Alkylating Agents
Environmental Exposure
Cell Differentiation
Pathology
Pregnancy
DNA

Keywords

  • MNU (methylnitrosourea)
  • alkylating agent
  • animal models
  • photoreceptor cells
  • retina
  • retinal degeneration
  • retinal dysplasia
  • teratology

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Retinal degeneration in the mouse. A model induced transplaceatally by methylnitrosourea. / Smith, Sylvia B; Yielding, K. Lemone.

In: Experimental Eye Research, Vol. 43, No. 5, 01.01.1986, p. 791-801.

Research output: Contribution to journalArticle

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