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Retinal degeneration and rd1 mutation in NC/Tnd mice-a human atopic dermatitis model
Kaoru Karasawa1, Akane Tanaka, Kyungsook Jung
1Laboratory of Veterinary Molecular Pathology and Therapeutics, Division of Animal Life Science, Graduate School, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo, Japan.
Purpose:
NC/Tnd mice, a spontaneous model for human atopic dermatitis, are also useful animal models for various corneal disorders accompanying allergic diseases. The purposes of the current study were to investigate the development of retinal degeneration in NC/Tnd mice.
Materials And Methods:
Histological examination was performed to determine time-dependent alterations of the retina in NC/Tnd from 8 to 28 days of age. Apoptotic cells were determined by TUNEL assay. Retinal function was examined by electroretinography. Fundoscopy was performed in NC/Tnd mice at 8 weeks of age. Melanin contents in whole-eye extracts were measured by spectrophotometry. Since the retinal degeneration 1 (rd1) mutation in the rod photoreceptor cyclic guanosine monophosphate phosphodiesterase 6 β-subunit (Pde6b(rd1)) has been identified in laboratory mice, the possible existence of the rd1 mutation was analyzed with PCR genotyping and gene sequencing. C57BL/6, WB, and C3H/HeN mice were used as controls.
Results:
Histological examination revealed rapid postnatal retinal degeneration in NC/Tnd mice. The number of apoptotic cells in the outer nuclear layer (ONL) increased with aging, and finally the ONL disappeared. Histological abnormality was not obvious in the inner nuclear layer or the ganglion cell layer. Electroretinography shows no response in adult NC/Tnd mice. Fundoscopic observation revealed hypopigmentation in the retina, and melanin contents in the eye were significantly reduced when compared with other inbred strains. Insertion in the rd1 allele was confirmed and a nonsense mutation of Pde6b(rd1) gene was determined in NC/Tnd mice.
Conclusions:
NC/Tnd mice also preserve the Pde6b(rd1) gene mutation resulting in the rapid postnatal retinal degeneration similar to that in C3H/HeN mice. Unlike C3H/HeN mice, since melanin contents of the retina in NC/Tnd mice was decreased, unknown defects may be present in the process of melanin composition in retinal pigment epithelial cells during fetal development of NC/Tnd mice.
Insights
NC/Tnd mice exhibit rapid postnatal retinal degeneration due to the Pde6b(rd1) gene mutation. These mice also show reduced retinal melanin, suggesting potential defects in melanin synthesis.
Area of Science:
- Ophthalmology
- Genetics
- Animal Models
Background:
- NC/Tnd mice are a model for human atopic dermatitis and associated corneal disorders.
- Retinal degeneration is a significant concern in various allergic diseases.
Purpose of the Study:
- To investigate the development of retinal degeneration in NC/Tnd mice.
- To identify the genetic basis and phenotypic characteristics of retinal changes in NC/Tnd mice.
Main Methods:
- Histological examination and TUNEL assay for apoptosis.
- Electroretinography for retinal function assessment.
- PCR genotyping and gene sequencing to analyze the Pde6b(rd1) mutation.
Main Results:
- Rapid postnatal retinal degeneration observed, with outer nuclear layer loss and increased apoptosis.
- Complete loss of retinal function in adult NC/Tnd mice.
- Confirmation of the Pde6b(rd1) gene mutation and reduced retinal melanin content.
Conclusions:
- NC/Tnd mice possess the Pde6b(rd1) mutation, causing rapid retinal degeneration similar to C3H/HeN mice.
- Decreased melanin content in NC/Tnd mice suggests potential defects in melanin synthesis during development.
- NC/Tnd mice serve as a valuable model for studying retinal degeneration linked to genetic mutations and pigment abnormalities.
