Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Case Report: The Endemic Spread of Escherichia coli Positive for Cytotoxic Necrotizing Factor Type 1 in a Canine Research Facility and Impact of Infection in Neonatal Puppies.

Journal of the American Association for Laboratory Animal Science : JAALAS·2025

Same author

Gene therapy advances using canine and feline animal models of inherited retinal degeneration.

Eye (London, England)·2025

Same author

Mapping the locus for ocular melanosis in Cairn Terriers.

Veterinary ophthalmology·2024

Same author

A combination treatment based on drug repurposing demonstrates mutation-agnostic efficacy in pre-clinical retinopathy models.

Nature communications·2024

Same author

Techniques for subretinal injections in animals.

Veterinary ophthalmology·2024

Same author

Consensus guidelines for nomenclature of companion animal inherited retinal disorders.

Veterinary ophthalmology·2024

Search research articles

Related Experiment Video

Updated: Aug 28, 2025

Author Spotlight: A Battery of Highly Reproducible Behavioral Tests to Validate an Angelman Syndrome Murine Model

Author Spotlight: A Battery of Highly Reproducible Behavioral Tests to Validate an Angelman Syndrome Murine Model

Published on: October 20, 2023

Residual rod function in CNGB1 mutant dogs.

Simon M Petersen-Jones¹, Nathaniel Pasmanter², Laurence M Occelli²

¹Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, 736 Wilson Road, D-208, East Lansing, MI, 48824, USA. peter315@msu.edu.

Documenta Ophthalmologica. Advances in Ophthalmology

|September 15, 2022

Summary

Mutations in CNGB1 cause retinitis pigmentosa. This study found that CNGB1 mutant dogs retain small, desensitized rod electroretinogram (ERG) responses, potentially due to low CNGA1 levels.

Keywords:

CNGB1 Dog-model Electroretinogram Retinitis pigmentosa Rod

More Related Videos

In Vivo Modeling of the Morbid Human Genome using Danio rerio

In Vivo Modeling of the Morbid Human Genome using Danio rerio

Published on: August 24, 2013

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

Related Experiment Videos

Last Updated: Aug 28, 2025

Author Spotlight: A Battery of Highly Reproducible Behavioral Tests to Validate an Angelman Syndrome Murine Model

Author Spotlight: A Battery of Highly Reproducible Behavioral Tests to Validate an Angelman Syndrome Murine Model

Published on: October 20, 2023

In Vivo Modeling of the Morbid Human Genome using Danio rerio

In Vivo Modeling of the Morbid Human Genome using Danio rerio

Published on: August 24, 2013

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

Area of Science:

Ophthalmology
Genetics
Neuroscience

Background:

Mutations in the cyclic nucleotide-gated (CNG) channel beta subunit (CNGB1) are a significant cause of recessive retinitis pigmentosa.
A novel large animal model with a truncating CNGB1 mutation was identified.

Purpose of the Study:

To investigate the electroretinogram (ERG) responses in a canine model with a CNGB1 mutation.
To characterize the residual rod function in CNGB1 mutant dogs.

Main Methods:

Dark-, light-adapted, and chromatic ERGs were recorded in CNGB1 mutant dogs and controls.
Comparisons were made with a rodless dog model (PDE6A-/-).
Immunohistochemistry was used to detect CNGA1 and CNGB1 subunits.

Main Results:

CNGB1 mutant dogs showed a raised ERG response threshold and lack of normal rod response, but retained cone responses.
A residual, desensitized rod ERG response was observed in CNGB1 mutant dogs, particularly at higher stimulus strengths.
Low levels of the CNGA1 subunit were detected in the outer segments of CNGB1 mutant dogs.

Conclusions:

CNGB1 mutant dogs exhibit residual ERG responses originating from desensitized rods.
This residual function may be attributed to the presence of low levels of CNGA1 in the outer segments.