Mobile Menu

  • AboutUs_Normal-24 The EyeCRO Approach
    • About Us
    • Careers
    • Location
    • Partners
  • MiDrops MiDROPS™
  • InVivo Models
    • Allergic Conjunctivitis
    • Corneal Sensitivity
    • Corneal Wound Healing
    • Diabetic Keratopathy
    • DL-AAA Retinal Leakage
    • Dry Eye Disease
    • Endotoxin induced Uveitis
    • Experimental Autoimmune Uveitis
    • Geographic Atrophy
    • Inherited Retinal Degenerations
    • Ischemia Reperfusion Injury
    • Laser-induced Choroidal Neovascularization
    • Light Damaged
    • Mitochondrial Neuropathy
    • Optic Nerve Crush
    • Oxygen Induced Retinopathy
    • Retinal Detachment
    • Retinal Vein Occlusion
    • STZ-induced Diabetic Retinopathy
    • VEGF-induced permeability
  • InVitro Capabilities
    • A2E Quantification
    • Bioanalytical Detection
    • Biochemistry
    • Histology
    • Ophthalmic Imaging and Physiology
  • News News
  • ContactUs Contact Us
  • Menu
  • Skip to primary navigation
  • Skip to main content

https://eyecro.com

  • AboutUs_Normal-24 The EyeCRO Approach
    • About Us
    • Careers
    • Location
    • Partners
  • MiDrops MiDROPS™
  • InVivo Models
    • Allergic Conjunctivitis
    • Corneal Sensitivity
    • Corneal Wound Healing
    • Diabetic Keratopathy
    • DL-AAA Retinal Leakage
    • Dry Eye Disease
    • Endotoxin induced Uveitis
    • Experimental Autoimmune Uveitis
    • Geographic Atrophy
    • Inherited Retinal Degenerations
    • Ischemia Reperfusion Injury
    • Laser-induced Choroidal Neovascularization
    • Light Damaged
    • Mitochondrial Neuropathy
    • Optic Nerve Crush
    • Oxygen Induced Retinopathy
    • Retinal Detachment
    • Retinal Vein Occlusion
    • STZ-induced Diabetic Retinopathy
    • VEGF-induced permeability
  • InVitro Capabilities
    • A2E Quantification
    • Bioanalytical Detection
    • Biochemistry
    • Histology
    • Ophthalmic Imaging and Physiology
  • News News
  • ContactUs Contact Us

Preclinical Ophthalmic Contract Research

Activation of the molecular chaperone, sigma 1 receptor, preserves cone function in a murine model of inherited retinal degeneration.

June 15, 2016 //  by stanselb

Retinal degenerative diseases are major causes of untreatable blindness, and novel approaches to treatment are being sought actively. Here we explored the activation of a unique protein, sigma 1 receptor (Sig1R), in the treatment of PRC loss because of its multifaceted role in cellular survival.  We used Pde6βrd10 (rd10) mice, which harbor a mutation in the rod-specific phosphodiesterase gene Pde6β and lose rod and cone photoreceptor cells (PRC) within the first 6 wk of life, as a model for severe retinal degeneration.  Systemic administration of the high-affinity Sig1R ligand (+)-pentazocine [(+)-PTZ] to rd10 mice over several weeks led to the rescue of cone function as indicated by electroretinographic recordings using natural noise stimuli and preservation of cone cells upon spectral domain optical coherence tomography and retinal histological examination.  The findings may have far-reaching therapeutic implications for retinal neurodegenerative diseases.

Read the entire article here.

Category: NewsTag: blindness, electroretinogram, OCT, ophthalmology research, optical coherence tomography, retina, retinal degeneration

Previous Post: « Prismatic eyewear for patients with tunnel vision to launch
Next Post: Roche CEO ‘sleeps better’ as risk to drugmaker’s growth recedes »

© 2023 · EyeCRO · All Rights Reserved.