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Dorette Z Ellis, Linya Li, Yang Liu, Shaoqing He, Thomas Yorio; Activation of Sigma-1 Receptor Restores Retinal Ganglion Cell Losses in Optic Nerve Crush Model for Glaucoma.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5296.
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© ARVO (1962-2015); The Authors (2016-present)
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 using wild-type mice.
ONC was performed in 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 intraperitoneally injecting the animals with pentazocine (PTZ; 0.5 mg/kg) 3 times weekly for the duration of the experiments. Additionally, two weeks prior to ONC, wildty type 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). Neuroprotective activities of the σ-1r were determined by counting RGCs in experimental animals.
RGC number was increased in wild-type ONC mice treated with PTZ when compared with untreated animals or σ-1r k/o mice. Wild-type ONC mice injected with AAV2-CAg-σ-1r-GFP vector demonstrated significant increases in RGC numbers and activity when compared with ONC mice injected with empty vector animals.
These findings suggest that over-expression or activation of σ-1rs provides neuroprotection of RGCs.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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