Development and aging of the eye in mice with inherited optic nerve aplasia

Histopathological studies

Jerry Silver, Stirling M. Puck, Daniel Albert

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

We have examined the morphological development of optic nerve aplasia in a subpopulation (10-20%) of anophthalmic mice (Strain ZRDCT-AN) that develop microphthalmia. During embryonic stages the optic fissure in microphthalmic mutants did not involute into the optic stalk. Even in the absence of a proper fissure, early differentiation of the various retinal elements was not disturbed. Subsequently, however, the optic nerve fibers failed to exit from the eye in their appropriate position. Secondary changes in the retina, probably resulting from a failure of optic axons to reach their central targets, were near total loss of ganglion cells and variable attenuation of the other nuclear and plexiform layers. Retinal rosettes were also commonly present.

Original languageEnglish (US)
Pages (from-to)257-266
Number of pages10
JournalExperimental Eye Research
Volume38
Issue number3
DOIs
StatePublished - Jan 1 1984
Externally publishedYes

Fingerprint

Optic Nerve
Microphthalmos
Nerve Fibers
Ganglia
Axons
Retina

Keywords

  • ganglion cell death
  • optic fissure malformation
  • optic nerve aplasia

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Development and aging of the eye in mice with inherited optic nerve aplasia : Histopathological studies. / Silver, Jerry; Puck, Stirling M.; Albert, Daniel.

In: Experimental Eye Research, Vol. 38, No. 3, 01.01.1984, p. 257-266.

Research output: Contribution to journalArticle

@article{897eb04103de48c287e7a71827bc99e5,
title = "Development and aging of the eye in mice with inherited optic nerve aplasia: Histopathological studies",
abstract = "We have examined the morphological development of optic nerve aplasia in a subpopulation (10-20{\%}) of anophthalmic mice (Strain ZRDCT-AN) that develop microphthalmia. During embryonic stages the optic fissure in microphthalmic mutants did not involute into the optic stalk. Even in the absence of a proper fissure, early differentiation of the various retinal elements was not disturbed. Subsequently, however, the optic nerve fibers failed to exit from the eye in their appropriate position. Secondary changes in the retina, probably resulting from a failure of optic axons to reach their central targets, were near total loss of ganglion cells and variable attenuation of the other nuclear and plexiform layers. Retinal rosettes were also commonly present.",
keywords = "ganglion cell death, optic fissure malformation, optic nerve aplasia",
author = "Jerry Silver and Puck, {Stirling M.} and Daniel Albert",
year = "1984",
month = "1",
day = "1",
doi = "10.1016/0014-4835(84)90164-7",
language = "English (US)",
volume = "38",
pages = "257--266",
journal = "Experimental Eye Research",
issn = "0014-4835",
publisher = "Academic Press Inc.",
number = "3",

}

TY - JOUR

T1 - Development and aging of the eye in mice with inherited optic nerve aplasia

T2 - Histopathological studies

AU - Silver, Jerry

AU - Puck, Stirling M.

AU - Albert, Daniel

PY - 1984/1/1

Y1 - 1984/1/1

N2 - We have examined the morphological development of optic nerve aplasia in a subpopulation (10-20%) of anophthalmic mice (Strain ZRDCT-AN) that develop microphthalmia. During embryonic stages the optic fissure in microphthalmic mutants did not involute into the optic stalk. Even in the absence of a proper fissure, early differentiation of the various retinal elements was not disturbed. Subsequently, however, the optic nerve fibers failed to exit from the eye in their appropriate position. Secondary changes in the retina, probably resulting from a failure of optic axons to reach their central targets, were near total loss of ganglion cells and variable attenuation of the other nuclear and plexiform layers. Retinal rosettes were also commonly present.

AB - We have examined the morphological development of optic nerve aplasia in a subpopulation (10-20%) of anophthalmic mice (Strain ZRDCT-AN) that develop microphthalmia. During embryonic stages the optic fissure in microphthalmic mutants did not involute into the optic stalk. Even in the absence of a proper fissure, early differentiation of the various retinal elements was not disturbed. Subsequently, however, the optic nerve fibers failed to exit from the eye in their appropriate position. Secondary changes in the retina, probably resulting from a failure of optic axons to reach their central targets, were near total loss of ganglion cells and variable attenuation of the other nuclear and plexiform layers. Retinal rosettes were also commonly present.

KW - ganglion cell death

KW - optic fissure malformation

KW - optic nerve aplasia

UR - http://www.scopus.com/inward/record.url?scp=0021348107&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021348107&partnerID=8YFLogxK

U2 - 10.1016/0014-4835(84)90164-7

DO - 10.1016/0014-4835(84)90164-7

M3 - Article

VL - 38

SP - 257

EP - 266

JO - Experimental Eye Research

JF - Experimental Eye Research

SN - 0014-4835

IS - 3

ER -