May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Fluocinolone Acetonide-Mediated Microglia Suppression in RCS Rat Model of Retinal Degeneration
Author Affiliations & Notes
  • R. Iezzi
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • A. Kennedy
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • I. Glybina
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • G. Abrams
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • Footnotes
    Commercial Relationships R. Iezzi, None; A. Kennedy, None; I. Glybina, None; G. Abrams, None.
  • Footnotes
    Support Ligon Research Center of Vision; Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3719. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      R. Iezzi, A. Kennedy, I. Glybina, G. Abrams; Fluocinolone Acetonide-Mediated Microglia Suppression in RCS Rat Model of Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3719.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Purpose:: We have previously shown that Fluocinolone Acetonide (FA), a synthetic steroid, is neuro-protective in the RCS rat model of retinal degeneration. The purpose of this study was to assess the role of FA-mediated microglial cell suppression in photoreceptor neuroprotection.

Methods:: Four groups of RCS rats (5 weeks old, 3 rats per group) were randomly assigned and implanted with intra-ocular, sustained-release FA devices as follows, 1.) 0.5 µg/day FA; 2.) 0.2 µg/day FA; 3.) inactive implant; 4.) untreated control. Electroretinograms (ERGs) were recorded pre-implantation and weekly, post-op. Rats were sacrificed at 9-weeks of age. The eyes were enucleated and retinas prepared as whole flat mounts or in transverse section and stained with antibodies against the microglial markers Iba-1, ED-1 and the macrophage marker, ED-2. Sections and whole mounts were examined by fluorescence microscopy and stained cells counted in standardized fields from all groups. Data were analyzed using one-way ANOVA, followed by multiple pairwise comparisons via the Tukey test.

Results:: In retinal whole mounts and sections, microglial cells were identified in four distinct layers by Iba-1 staining, corresponding to an inner layer (IL), adjacent to the retinal ganglion cells, a middle layer (ML), a layer at the photoreceptors (PL) and a layer within the outer-debris zone (DL). Mean IL, PL and DL microglial cell counts were significantly lower in FA-treated eyes as compared to placebo controls (p<0.002). Treated eyes of both FA groups demonstrated 43% fewer PL microglia on IBA-1 sections. Microglial cells in FA-treated groups also had a more "tuberous" morphology compared to the amoeboid characteristics of activated cells. In transverse sections labelled with ED-1 antibody for activated microglia, staining was seen within the DL, only. FA-treated groups demonstrated an 87% reduction in the number of activated DL- microglial cells (p=0.001). All retinal preparations were uniformly negative for ED-2, indicating that staining was not due to infiltration of blood-borne macrophages into the retina.

Conclusions:: FA has profound effects on retinal microglia. FA reduced overall microglial cell counts as well as the number of activated microglia. In addition, FA-treated microglia assumed an inactive morphology. Anti-inflammatory Microglial Suppression Therapy (MST) may provide an approach to the treatment of patients with retinal neurodegenerative diseases such as Retinitis Pigmentosa and Age-Related Macular Degeneration.

Keywords: retina • microglia • degenerations/dystrophies 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.