April 2014
Volume 55, Issue 13
ARVO Annual Meeting Abstract  |   April 2014
Delta Opioid-Receptors activation mitigates detrimental effects of TNF-α during Retinal Ganglion Cells Degeneration.
Author Affiliations & Notes
  • Yasir Abdul
    Ophthalmology, Medical Univ of South Carolina, Charleston, SC
  • Matthew J Nutaitis
    Ophthalmology, Medical Univ of South Carolina, Charleston, SC
  • Shahid Husain
    Ophthalmology, Medical Univ of South Carolina, Charleston, SC
  • Footnotes
    Commercial Relationships Yasir Abdul, None; Matthew Nutaitis, None; Shahid Husain, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1899. doi:
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      Yasir Abdul, Matthew J Nutaitis, Shahid Husain; Delta Opioid-Receptors activation mitigates detrimental effects of TNF-α during Retinal Ganglion Cells Degeneration.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1899.

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

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Purpose: To determine if TNF-α causes a direct injury to the retinal ganglion cells (RGCs) and TNF-α-induced RGCs injury is alleviated by the activation of delta opioid-receptors.

Methods: TNF-α was injected intravitreally (10 ng TNF-α in 3µl) in deeply anesthetized Brown Norway rats. Contralateral eye was used as sham or control and injected with vehicle (3 µl PBS). Animals were treated with a selective delta opioid-receptor agonist (SNC-121; 1mg/kg; i.p) right after the intravitreal injection of TNF-α and subsequently daily for 7 days. Intraocular Pressure (IOP) was measured as the average of 6-8 consecutive measurements prior to surgery (baseline IOP) and weekly after TNF-α injection for 28 days. Functional response of RGCs and retina was measured by pattern electroretinograms (Pattern-ERGs) and scotopic-ERGs, respectively. Retinal ganglion cells (RGCs) were visualized by retrograde-labeling using fluorogold. Optic nerve morphology was determined by toluidine blue staining in optic nerve head sections.

Results: The intraocular pressure was neither changed in vehicle nor in TNF-α treated animal. The pattern-ERGs were reduced by 44% in TNF-α treated eyes on day 28th when compared with vehicle treated eyes (Sham eyes 100 ± 00% vs TNF-α treated eyes 66 ± 7%; p<0.05). The loss in pattern-ERGs was significantly reduced in SNC-121 treated groups (TNF-α treated eyes 66 ± 7% vs SNC-121 + TNF-α treated eyes 98 ± 11%; p<0.05). In addition to pattern-ERGs, scotopic-ERGs were also improved in SNC-121 treated group when measured on day 28th, post injury. The numbers of RGCs were reduced significant (p<0.05) in TNF-α treated eyes, which was improved in the presence of SNC-121. Additionally, TNF-α treatment causes morphological changes and axonal loss, which was preserved by SNC-121 treatment.

Conclusions: We have shown earlier that TNF-α is produced from glial cells very early during the progression of glaucoma, which subsequently lead to the RGC death. Current data supported our previous findings and provide new evidences that TNF-α caused direct injury to the axons and RGCs. Additionally, we have shown that activation of delta opioid-receptors by exogenous ligand rescue axons and RGCs against TNF-α-induced retinal injury.

Keywords: 615 neuroprotection • 629 optic nerve • 695 retinal degenerations: cell biology  

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