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MGI - Inbred Strains: STR

Inbred Strains of Mice: STR

Inbr (N) 145. Brown

Origin: Strong from a stock treated with methylcholanthrene between generations F4 and F27.

Susceptible to periodontal disease. Polydipsia with the daily water intake of the polydipsic STR/N of both sexes being between five and eight times that of nonpolydipsic controls: STR/1N, and Swiss-Webster (S/W) mice. Polydipsia may depend, at least in part, on the angiotensin II system in the brain. (

). Susceptible to periodontal disease (

., 1961); polydipsic.

Inbr (N) 138. Piebald brown.

Origin: piebald mutation in STR at F29 in 1961. Develops osteoarthropathy of the knee joints, and obstructive uropathy in males before 16 months. Maint. by N.

Osteoarthropathy of the knee joints (

). The condition has been considered in detail by Walton 1977a, b, 1979 a, b, c). Oseroarthrosis is a non-inflammatory disease in which there is degeneration if the articulating surfaces of a joint with associated thickening of the underlying bone. By around 12 months of age 60% of males and 30% of females have osteoarthrosis as assessed radiologically. Medial patella dislocation, which can be prevented by surgical stabilization of the patella leading to a reduction in the disease, is a common feature of the condition. Eventually, the conditions becomes so severe as to impair joint movement.

Up to 90% of male mice develop osteoarthritis which is related to changes in monoamine oxidase activity and distribution, and catecholamine metabolism. Simultaneous treatment with both diclofenac sodium and tribenoside resulted in 7/9 mice having no sign of osteoarthritis (Chayen et al, 1996).

Changes in the patellar tendon of males were observed at five months using magnetic resonance imaging. Other degenerative features were seen at nine months (Munasinghe et al, 1996).

High level of plasma phospholipids, cholesterol, cholesterol ester and total lipids, but no excessive obesity (Yamamoto et al., 1963., 1963). Sokoloff et al (1962) considered that the mice become obese, but Walton (1979a) found that males were not obese when compared with CBA, though females were, and did not consider that obesity was associated with the osteoarthropathy. Polydipsia (Bernstein, 1966) and obstructive uropathy constantly seen at less than 16 months (Russell and Meier, 1966). Urine has low osmolality (7/7) (Silverstein, 1961).

Bernstein S. E. (1966) Physiological characteristics, in Biology of the Laboratory Mouse, 2nd. ed. (Green E. L., ed), pp. 337-350. McGraw-Hill, New York.

Chayen J., Bitensky L., and Chambers M. G. (1996) Modulation of murine osteoarthritis. Cell Biochemistry and Function 14, 57-61.

Katafuchi T., Hattori Y., Nagatomo I., Koizumi K., and Silverstein E. (1991) Involvement of angiotensin II in water intake of genetically polydipsic mice. Am. J. Physiol. 260, R1152-R1158.

Munasinghe J. P., Tyler J. A., Hodgson R. J., Barry M. A., Gresham G. A., Evans R., and Hall L. D. (1996) Magnetic resonance imaging, histology, and X-ray of three stages of damage to the knees of SRT/ORT mice. Investigative Radiology 31, 630-638.

Russell E. S. and Meier H. (1966) Constitutional diseases, in Biology of the Laboratory Mouse, 2nd. ed. (Green E. L., ed), pp. 571-587. McGraw-Hill, New York.

Silverstein E. (1961) Urine specific gravity and osmolality in inbred strains of mice. J. Appl. Physiol. 16, 194-196.

Sokoloff L., Crittenden L., Yamamoto R., and Jay G. E. (1962) The genetics of degenerative joint disease in mice. Arthritis Rheum. 5, 531-564.

Walton M. (1979a) Bone thickening in osteoarthrosis. Acta Orthop. Scand. 50, 501-506.

Yamamoto R. S., Crittenden L. B., Sokoloff L., and Jay G. E. (1963) Genetic variations in plasma lipid content in mice. J. Lipid Res. 4, 413-418.

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