Chronology of optic nerve head and retinal responses to elevated intraocular pressure

Elaine Johnson, Lisa M H Deppmeier, Susan K F Wentzien, Immanuel Hsu, John Morrison

Research output: Contribution to journalArticle

181 Citations (Scopus)

Abstract

Purpose. To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). Methods. After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation. Results. Mean IOP for the experimental eyes was 36 ± 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain- derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells. Conclusions. Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.

Original languageEnglish (US)
Pages (from-to)431-442
Number of pages12
JournalInvestigative Ophthalmology and Visual Science
Volume41
Issue number2
StatePublished - 2000

Fingerprint

Chronology
Optic Disk
Intraocular Pressure
Retinal Ganglion Cells
Nerve Growth Factors
Retina
Pressure
Apoptosis
Connexin 43
Glial Fibrillary Acidic Protein
Brain-Derived Neurotrophic Factor
DNA Fragmentation
Optic Nerve
Neuroglia
Ganglia
Blood Vessels
Reference Values
Collagen
Staining and Labeling

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Chronology of optic nerve head and retinal responses to elevated intraocular pressure. / Johnson, Elaine; Deppmeier, Lisa M H; Wentzien, Susan K F; Hsu, Immanuel; Morrison, John.

In: Investigative Ophthalmology and Visual Science, Vol. 41, No. 2, 2000, p. 431-442.

Research output: Contribution to journalArticle

@article{103dda761b414035900e808097a9328c,
title = "Chronology of optic nerve head and retinal responses to elevated intraocular pressure",
abstract = "Purpose. To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). Methods. After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation. Results. Mean IOP for the experimental eyes was 36 ± 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain- derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells. Conclusions. Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.",
author = "Elaine Johnson and Deppmeier, {Lisa M H} and Wentzien, {Susan K F} and Immanuel Hsu and John Morrison",
year = "2000",
language = "English (US)",
volume = "41",
pages = "431--442",
journal = "Investigative Ophthalmology and Visual Science",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
number = "2",

}

TY - JOUR

T1 - Chronology of optic nerve head and retinal responses to elevated intraocular pressure

AU - Johnson, Elaine

AU - Deppmeier, Lisa M H

AU - Wentzien, Susan K F

AU - Hsu, Immanuel

AU - Morrison, John

PY - 2000

Y1 - 2000

N2 - Purpose. To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). Methods. After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation. Results. Mean IOP for the experimental eyes was 36 ± 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain- derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells. Conclusions. Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.

AB - Purpose. To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). Methods. After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation. Results. Mean IOP for the experimental eyes was 36 ± 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain- derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells. Conclusions. Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.

UR - http://www.scopus.com/inward/record.url?scp=0033950441&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033950441&partnerID=8YFLogxK

M3 - Article

VL - 41

SP - 431

EP - 442

JO - Investigative Ophthalmology and Visual Science

JF - Investigative Ophthalmology and Visual Science

SN - 0146-0404

IS - 2

ER -