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  • Model #
  • Genotype
  • Nomenclature
  • NMRI-F
  • NMRI-M
  • Extensively used as an experimental animal in many fields of general biology as well as in pharmacology and toxicology
  • Commonly used as a control for selection experiments
  • Develops a wide variety of spontaneous tumors and an increasing incidence of renal disease with age
Origin: The NMRI outbred model was developed by Lynch et al. Poiley of the National Institutes of Health received stock from Lynch in 1937. The mice were inbred as NIH/P1. The Naval Medical Research Institute (NMRI) received stock from Lynch. Zentralinstitut für Versuchstierzucht in Hannover Germany (Han) received stock from NMRI. The mice were random bred. M&B A/S (now Taconic Europe) received stock from Han in 1961 and again in 1985. The mice are maintained as an outbred stock.

Genetics: Immunology: H2q

Coat Color Loci: A/a, Tyrc

Species: Mouse

Color: Albino

Average litter size: 10

Life-span of males short in conventional conditions (430 days) but long in females (750 days) (Storer, 1966). Life-span in SPF fostered conditions also short in males (490 days) and long in females (690 days) (Festing and Blackmore, 1971).

Spontaneous glomerulonephritis occurs in the NMRI mouse stock at a relatively high incidence. In a study concerning spontaneous diseases in NMRI mice, glomerulonephritis was found to account for severe illness in 27.2% of the cases (Deerberg F & Müller-Peddinghaus 1970). The frequency of histologically proven glomerulonephritis increases with age reaching a frequency of 43.8 % at 22-24 months.

In 95.2 % of all the cases of glomerulonephritis two or more of the four employed immunoglobulin classes and subclasses (IgG1, IgG2, IgA, and IgM) can be detected by immunoflourescence. Glomerular deposit of IgG starts at an age of 6 month and increases with age.

The histological picture of glomerulonephritis includes cell proliferation in the glomeruli, deposit of PAS-positive substance and increase in the mesangial matrix. In the final stages of the disease fibrosis in the glomeruli and lesions in the tubuli and interstitium are found. Clinical symptoms are limited until the final stage which is characterised by ascites and massive edema. Increased proteinuria is seen in some animals during the development of the disease (Deerberg & Gleichman 1980).

Antinuclear antibodies or antiboides against erythrocytes are not found in connection with the development of glomerulonephritis in NMRI mice in contrast to the glomerulonephritis in ZBWF1 and MRL/Mp-lpr mice which serve as the animal model for the human disease (Deerberg & Gleichman 1980).

Application in Biomedical Research:
The NMRI mouse is widely used as an experimental animal in many fields of general biology as well as in pharmacology and toxicology. NMRI mice may serve as a base population for a selection experiment, in which case it is especially desirable to perpetuate a random bred line as a control. Furthermore, they may serve as a population harboring deleterious mutations.

Traditionally random bred laboratory animals have been used extensively in toxicological studies, because they have been said to have a degree of variance similar to what would be expected in the human population. However, outbred stocks are genetically variable to the extent that all individuals are genetically unique, but they tend to be relatively uniform in comparison with the variability within the species. The toxicological testing of a compound in a single stock of outbred animals can be said to be equivalent, genetically, to doing clinical trials in an isolated human population such as certain groups of Eskimos, Bushmen, etc.

An alternative strategy for testing would be to use a number of different inbred strains of the same species, the so-called factorial experiment. This could be done by carrying out the animal tests on a sample of five to ten inbred strains. The advantages of this strategy would be that the factorial experiment, still using the same number of animals as in the classical design, would include a wider range of phenotype variations within the test species thus indicating whether the response to the drug is under genetic control. In this way the test would be statistically more powerful. (Festing 1979, Festing 1987, Shimkin 1974, Haseman & Hoel 1973).