June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Activation of Sigma-1 Receptor Protects Retinal Ganglion Cell Loss in Optic Nerve Crush Model for Glaucoma
Author Affiliations & Notes
  • Dorette Z Ellis
    UNT System College of Pharmacy, Fort Worth, Texas, United States
    NTERI, UNTHSC, Fort Worth, Texas, United States
  • Linya Li
    UNT System College of Pharmacy, Fort Worth, Texas, United States
  • Shaoqing He
    NTERI, UNTHSC, Fort Worth, Texas, United States
  • Yang Liu
    NTERI, UNTHSC, Fort Worth, Texas, United States
  • Thomas Yorio
    NTERI, UNTHSC, Fort Worth, Texas, United States
  • Footnotes
    Commercial Relationships   Dorette Ellis, None; Linya Li, None; Shaoqing He, None; Yang Liu, None; Thomas Yorio, None
  • Footnotes
    Support  UNTHSC Funds
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 212. doi:
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    • Get Citation

      Dorette Z Ellis, Linya Li, Shaoqing He, Yang Liu, Thomas Yorio; Activation of Sigma-1 Receptor Protects Retinal Ganglion Cell Loss in Optic Nerve Crush Model for Glaucoma. Invest. Ophthalmol. Vis. Sci. 2017;58(8):212.

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

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Abstract

Purpose : Recent studies in sigma-1 receptors (σ-1r) deficient (k/o) mice demonstrated increased losses of retinal ganglion cells (RGCs) in oxidative stress and optic nerve crush mice models (ONC). This study determines the neuroprotective role of the σ-1r in ONC model.

Methods : ONC was performed in σ-1r k/o mice and wild type mice. Briefly, the left optic nerve (ON) was exposed intraorbitally through a small window made between the surrounding muscles. The ON was crushed approximately 1mm behind the globe with self-closing forceps for 4 seconds under visualization. The contralateral eye was used as controls for ONC and σ-1r k/o mice served as controls for off receptor action. The σ-1r was activated by the intraperitoneal injection with pentazocine (PTZ; 0.5 mg/kg) 3x weekly for the duration of the experiments. Additionally, two weeks prior to ONC, mice were intravitreally injected with AAV2-CAg-σ-1r-GFP vector and expression of σ-1r was assessed; AAV2 empty vector served as controls. RGC activity was measured using pattern electroretinogram (pERG). Termination experiments included counting RGCs in experimental animals to determine neuroprotective activities of the σ-1r.

Results : RGC death was decreased in wild-type mice treated with PTZ when compared with σ-1r k/o or untreated animals. σ-1r k/o ONC mice injected with AAV2-CAg-σ-1r-GFP vector demonstrated significant increases in RGCs numbers and activity when compared with σ-1r k/o ONC mice injected with empty vector or non-injected σ-1r k/o ONC animals.

Conclusions : Our studies indicate that expression or activation of σ-1rs provides neuroprotection of RGCs.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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