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Malinda E. Fitzgerald, Corey Haughey, Nobel Del Mar, Anton J. Reiner; Increased Retinal Müller Cell Immunolabeling For Glial Fibrillary Acidic Protein In Rats Following Either Impairment Of Sympathetic Control Of Choroidal Blood Flow By Removal Of The Superior Cervical Ganglion Or By Normal Aging. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2006.
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© ARVO (1962-2015); The Authors (2016-present)
The Superior Cervical Ganglion (SCG) is the source of the vasoconstrictory sympathetic innervation of choroidal vessels. Impaired sympathetic control of choroid results in a failure of baroregulatory vasoconstriction of choroidal vessels, and thus excessive choroidal blood flow (ChBF) during high blood pressure. We have shown previously that disruption of adaptive parasympathetic control of choroid during low systemic blood pressure impairs retinal function as assessed by ERG, and increases glial fibrillary acidic protein (GFAP) in retinal Müller cells (ARVO e abstract 4081, 2011). In this current study, we characterized retinal pathology using GFAP immunohistochemistry following removal of the SCG. We also investigated GFAP immunolabelling in retina in normal aging.
Retinal morphology was examined in 26 rats. Thirteen rats served as young controls and either received no removal of the SCG or an electrolytic lesion in a brain region unrelated to sympathetic or parasympathetic ChBF control. Eleven rats received bilateral SCG-ectomies and were allowed to recover for 4-8 weeks. Four rats greater than a year old were also studied. Paraformaldehyde-perfusion fixed retinas were sectioned on a cryostat (20µm), slide-mounted, and immunolabeled for GFAP using peroxidase-antiperoxidase methods with diaminobenzidine. GFAP immunolabeling was blindly analyzed as to group category using a scoring system that reflected the extent of GFAP labeling in the Müller cells and the abundance of labeled Müller cells.
The retinas from SCG-ectomy rats showed a significant increase in GFAP immunolabeling within the retina in comparison with retinas from control rats, with the SCG-ectomy levels being more than 2x those in controls. A similar GFAP increase was previously seen following disruption of parasympathetic ChBF control (ARVO e abstract 4081, 2011). The old rats had GFAP levels 3.5x those in controls.
Müller cells of the retina respond to ChBF deficiency caused by disrupted sympathetic choroidal regulation, as they also do to disruption of the parasympathetic control. These findings indicate that both the sympathetic and parasympathetic regulation of ChBF play an important role in maintaining retinal health. The basis of the great retinal GFAP increase with aging is uncertain, but age-related changes in sympathetic and parasympathetic regulation of ChBF may be contributors.
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