title: Glial Cell Contribution to Basal Vessel Diameter and Pressure-Initiated Vascular Responses in Rat Retina.
abstract: The purpose of this study was to test the hypothesis that retinal glial cells modify basal vessel diameter and pressure-initiated vascular regulation in rat retina.
  
  
  
  In rats, L-2-aminoadipic acid (LAA, 10 nM) was intravitreally injected to inhibit glial cell activity. Twenty-four hours following injection, retinal glial intracellular calcium (Ca2+) was labeled with the fluorescent calcium indicator Fluo-4/AM (F4, 1 mM). At 110 minutes after injection, intraocular pressure (IOP) was elevated from 20 to 50 mm Hg. Prior to and during IOP elevation, Ca2+ and retinal vessel diameter were assessed using a spectral-domain optical coherence tomography/confocal scanning laser ophthalmoscope. Dynamic changes in Ca2+ and diameter from IOP elevation were quantified. The response in LAA-treated eyes was compared with vehicle treated control eyes.
  
  
  
  L-2-Aminoadipic acid treatment significantly reduced F4-positive cells in the retina (LAA, 16 ± 20 vs. control, 55 ± 37 cells/mm2; P = 0.02). Twenty-four hours following LAA treatment, basal venous diameter was increased from 38.9 ± 3.9 to 51.8 ± 6.4 μm (P < 0.0001, n = 20), whereas arterial diameter was unchanged (from 30.3 ± 3.5 to 30.7 ± 2.8 μm; P = 0.64). In response to IOP elevation, LAA-treated eyes showed a smaller increase in glial cell Ca2+ around both arteries and veins in comparison with control (P < 0.001 for both). There was also significantly greater IOP-induced vasoconstriction in both vessel types (P = 0.05 and P = 0.02, respectively; n = 6 each).
  
  
  
  The results suggest that glial cells can modulate basal retinal venous diameter and contribute to pressure-initiated vascular responses.
authors.affiliation: Department of Ophthalmology, The Tenth People's Hospital, Shanghai, Tongji University School of Medicine, Shanghai, China 2Devers Eye Institute, Legacy Research Institute, Portland, Oregon, USA.
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Optometry and Vision Sciences, University of Melbourne, Parkville, Victoria, Australia.
authors.forename: Bang V
authors.initials: BV
authors.lastname: Bui
authors.affiliation: Devers Eye Institute, Legacy Research Institute, Portland, Oregon, USA.
authors.forename: Grant
authors.initials: G
authors.lastname: Cull
authors.affiliation: Department of Ophthalmology, The Tenth People's Hospital, Shanghai, Tongji University School of Medicine, Shanghai, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Wang
authors.affiliation: Department of Ophthalmology, The Tenth People's Hospital, Shanghai, Tongji University School of Medicine, Shanghai, China 2Devers Eye Institute, Legacy Research Institute, Portland, Oregon, USA.
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007429:Intraocular Pressure / Q000502:physiology*; D008297:Male; D009457:Neuroglia / Q000473:pathology*; D009798:Ocular Hypertension / Q000473:pathology / Q000503:physiopathology*; D009887:Ophthalmoscopy; D009898:Optic Disk / Q000098:blood supply*; D051381:Rats; D011914:Rats, Inbred BN; D012039:Regional Blood Flow / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000473:pathology; D012171:Retinal Vessels / Q000473:pathology / Q000503:physiopathology*; D041623:Tomography, Optical Coherence / Q000379:methods*; D014661:Vasoconstriction / Q000502:physiology*