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Related Experiment Video

Updated: Jul 4, 2026

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
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Published on: July 14, 2016

Sigma1 Receptor Activation Confers Durable Neuroprotection Following Neonatal Ischemic Retinal Injury.

Jing Wang1,2, Xiaowen Lu1,2, Zhengyu Lu1

  • 1Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA.

Research Square
|July 3, 2026
PubMed
Summary

Activating Sigma 1 receptor (Sig1R) protects against vision loss in retinopathy of prematurity (ROP) by preserving retinal structure and function. This receptor-dependent neuroprotection offers a promising therapeutic avenue for preventing childhood blindness.

Keywords:
Retinopathy of prematuritySigma 1 receptormitochondrial dysfunctionneuroprotectionoxidative stressoxygen-induced retinopathyretinal neurodegeneration

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Pharmacology

Background:

  • Retinopathy of prematurity (ROP) is a major cause of childhood blindness.
  • Current ROP therapies address neovascularization but not persistent visual dysfunction.
  • Neuroprotective strategies are needed to preserve long-term vision in ROP patients.

Purpose of the Study:

  • To investigate the neuroprotective potential of Sigma 1 receptor (Sig1R) activation in a mouse model of neonatal ischemic retinal injury.
  • To determine if Sig1R activation confers sustained protection against structural and functional deficits in retinopathy of prematurity (ROP).

Main Methods:

  • Oxygen-induced retinopathy (OIR) model in wild-type and Sig1R knockout mice.
  • Systemic administration of the Sig1R agonist (+)-pentazocine [(+)-PTZ].
  • Longitudinal assessment of visual function (visual acuity, contrast sensitivity, ERG, PERG) and retinal structure (SD-OCT, histology).

Main Results:

  • Chronic Sig1R activation significantly improved visual acuity, contrast sensitivity, and retinal function in OIR mice.
  • Sig1R activation preserved retinal ganglion cell survival and inner retinal architecture.
  • Protective effects were abolished in Sig1R-deficient mice, confirming receptor dependence.
  • Mechanism involved reduced apoptosis, oxidative stress, and improved mitochondrial function.

Conclusions:

  • Sig1R activation provides sustained, receptor-dependent neuroprotection against neonatal ischemic retinal injury.
  • This protection is mediated by coordinated regulation of redox, mitochondrial, and cell-survival pathways.
  • Sig1R represents a promising therapeutic target for preserving retinal integrity and visual function in retinopathy of prematurity.