Evidence for retinal pathology following interruption of neural regulation of choroidal blood flow

Müller cells express GFAP following lesions of the nucleus of edinger-westphal in pigeons

Malinda E.C. Fitzgerald, Betty A. Vana, Anton Reiner

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Abstract

Choroidal blood flow in pigeons is regulated by the medial part of the nucleus of Edinger-Westphal (EW) via the ipsilateral ciliary ganglion. Interruption of this circuit by unilateral lesions of EW results in pathological modifications in the morphology of retinal photoreceptors in the ipsilateral eye in pigeons housed under 12hr light (400 lux)/12hr dark conditions. In the present study, we examined the effects of unilateral EW lesions on glial fibrillary acidic protein (GFAP) expression by retinal Müller cells in pigeons housed under the same lighting conditions. Since Müller cells in the retina of land vertebrates express increased GFAP during conditions of retinal pathology or stress (e.g., inflammation or hypoxia), this study would enable us to further evaluate the effects of disruption in the neural regulation of choroidal blood flow on the retina. We found that following EW lesions, retinal Müller cells expressed GFAP, with the precise intracellular location of the GFAP dependent on the amount of time elapsed following the lesion. One week after the EW lesions, GFAP labelling was restricted to the Müller cell endfeet in the nerve fiber layer and ganglion cell layer. By two-three weeks, the labelling had extended outward (or sclerad) into the portions of the Müller cells spanning the inner plexiform layer. Finally, by six weeks post-lesion, the entire extent of the Müller cell from the nerve fiber layer to the outer limiting membrane contained GFAP. No GFAP immunoreactivity in Müller cells was observed in the eyes contralateral to the EW lesions or in eyes in which the pupil had been fixed and dilated by lesions of the pretectal region. Our results suggest that the retina is in a state of physiological stress following interruption of the neural regulation of choroidal blood flow by EW lesions. Although the precise mechanisms by which altered choroidal blood flow regulation affects Müller cell GFAP production require elucidation, the results nonetheless highlight the importance of intact neural regulation of choroidal blood flow for retinal health.

Original languageEnglish (US)
Pages (from-to)583-598
Number of pages16
JournalCurrent Eye Research
Volume9
Issue number6
DOIs
StatePublished - Jan 1 1990

Fingerprint

Glial Fibrillary Acidic Protein
Columbidae
Pathology
Retina
Nerve Fibers
Parasympathetic Ganglia
Edinger-Westphal Nucleus
Vertebrate Photoreceptor Cells
Physiological Stress
Pupil
Lighting
Ganglia
Vertebrates
Inflammation
Light
Membranes
Health

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

@article{edf92a1e9e4a4ee1a716ce79703cef0e,
title = "Evidence for retinal pathology following interruption of neural regulation of choroidal blood flow: M{\"u}ller cells express GFAP following lesions of the nucleus of edinger-westphal in pigeons",
abstract = "Choroidal blood flow in pigeons is regulated by the medial part of the nucleus of Edinger-Westphal (EW) via the ipsilateral ciliary ganglion. Interruption of this circuit by unilateral lesions of EW results in pathological modifications in the morphology of retinal photoreceptors in the ipsilateral eye in pigeons housed under 12hr light (400 lux)/12hr dark conditions. In the present study, we examined the effects of unilateral EW lesions on glial fibrillary acidic protein (GFAP) expression by retinal M{\"u}ller cells in pigeons housed under the same lighting conditions. Since M{\"u}ller cells in the retina of land vertebrates express increased GFAP during conditions of retinal pathology or stress (e.g., inflammation or hypoxia), this study would enable us to further evaluate the effects of disruption in the neural regulation of choroidal blood flow on the retina. We found that following EW lesions, retinal M{\"u}ller cells expressed GFAP, with the precise intracellular location of the GFAP dependent on the amount of time elapsed following the lesion. One week after the EW lesions, GFAP labelling was restricted to the M{\"u}ller cell endfeet in the nerve fiber layer and ganglion cell layer. By two-three weeks, the labelling had extended outward (or sclerad) into the portions of the M{\"u}ller cells spanning the inner plexiform layer. Finally, by six weeks post-lesion, the entire extent of the M{\"u}ller cell from the nerve fiber layer to the outer limiting membrane contained GFAP. No GFAP immunoreactivity in M{\"u}ller cells was observed in the eyes contralateral to the EW lesions or in eyes in which the pupil had been fixed and dilated by lesions of the pretectal region. Our results suggest that the retina is in a state of physiological stress following interruption of the neural regulation of choroidal blood flow by EW lesions. Although the precise mechanisms by which altered choroidal blood flow regulation affects M{\"u}ller cell GFAP production require elucidation, the results nonetheless highlight the importance of intact neural regulation of choroidal blood flow for retinal health.",
author = "Fitzgerald, {Malinda E.C.} and Vana, {Betty A.} and Anton Reiner",
year = "1990",
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T1 - Evidence for retinal pathology following interruption of neural regulation of choroidal blood flow

T2 - Müller cells express GFAP following lesions of the nucleus of edinger-westphal in pigeons

AU - Fitzgerald, Malinda E.C.

AU - Vana, Betty A.

AU - Reiner, Anton

PY - 1990/1/1

Y1 - 1990/1/1

N2 - Choroidal blood flow in pigeons is regulated by the medial part of the nucleus of Edinger-Westphal (EW) via the ipsilateral ciliary ganglion. Interruption of this circuit by unilateral lesions of EW results in pathological modifications in the morphology of retinal photoreceptors in the ipsilateral eye in pigeons housed under 12hr light (400 lux)/12hr dark conditions. In the present study, we examined the effects of unilateral EW lesions on glial fibrillary acidic protein (GFAP) expression by retinal Müller cells in pigeons housed under the same lighting conditions. Since Müller cells in the retina of land vertebrates express increased GFAP during conditions of retinal pathology or stress (e.g., inflammation or hypoxia), this study would enable us to further evaluate the effects of disruption in the neural regulation of choroidal blood flow on the retina. We found that following EW lesions, retinal Müller cells expressed GFAP, with the precise intracellular location of the GFAP dependent on the amount of time elapsed following the lesion. One week after the EW lesions, GFAP labelling was restricted to the Müller cell endfeet in the nerve fiber layer and ganglion cell layer. By two-three weeks, the labelling had extended outward (or sclerad) into the portions of the Müller cells spanning the inner plexiform layer. Finally, by six weeks post-lesion, the entire extent of the Müller cell from the nerve fiber layer to the outer limiting membrane contained GFAP. No GFAP immunoreactivity in Müller cells was observed in the eyes contralateral to the EW lesions or in eyes in which the pupil had been fixed and dilated by lesions of the pretectal region. Our results suggest that the retina is in a state of physiological stress following interruption of the neural regulation of choroidal blood flow by EW lesions. Although the precise mechanisms by which altered choroidal blood flow regulation affects Müller cell GFAP production require elucidation, the results nonetheless highlight the importance of intact neural regulation of choroidal blood flow for retinal health.

AB - Choroidal blood flow in pigeons is regulated by the medial part of the nucleus of Edinger-Westphal (EW) via the ipsilateral ciliary ganglion. Interruption of this circuit by unilateral lesions of EW results in pathological modifications in the morphology of retinal photoreceptors in the ipsilateral eye in pigeons housed under 12hr light (400 lux)/12hr dark conditions. In the present study, we examined the effects of unilateral EW lesions on glial fibrillary acidic protein (GFAP) expression by retinal Müller cells in pigeons housed under the same lighting conditions. Since Müller cells in the retina of land vertebrates express increased GFAP during conditions of retinal pathology or stress (e.g., inflammation or hypoxia), this study would enable us to further evaluate the effects of disruption in the neural regulation of choroidal blood flow on the retina. We found that following EW lesions, retinal Müller cells expressed GFAP, with the precise intracellular location of the GFAP dependent on the amount of time elapsed following the lesion. One week after the EW lesions, GFAP labelling was restricted to the Müller cell endfeet in the nerve fiber layer and ganglion cell layer. By two-three weeks, the labelling had extended outward (or sclerad) into the portions of the Müller cells spanning the inner plexiform layer. Finally, by six weeks post-lesion, the entire extent of the Müller cell from the nerve fiber layer to the outer limiting membrane contained GFAP. No GFAP immunoreactivity in Müller cells was observed in the eyes contralateral to the EW lesions or in eyes in which the pupil had been fixed and dilated by lesions of the pretectal region. Our results suggest that the retina is in a state of physiological stress following interruption of the neural regulation of choroidal blood flow by EW lesions. Although the precise mechanisms by which altered choroidal blood flow regulation affects Müller cell GFAP production require elucidation, the results nonetheless highlight the importance of intact neural regulation of choroidal blood flow for retinal health.

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