of Mice: STR
Inbr (N) 145. Brown a,b.
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. (Katafuchi et al 1991
Susceptible to periodontal disease (Baer et
., 1961); polydipsic.
STR/1 and STR/Ort
Inbr (N) 138. Piebald brown. a,b,s.
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 (Russell
and Meier, 1966
). 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).
Baer P. N.,
Crittenden L. B., Jay G. E. Jr., and Lieberman J. E. (1961) Studies on
periodontal disease in the mouse. II. Genetic and maternal effects. J.
Dental Res. 40, 23-33.
E. (1966) Physiological characteristics, in Biology of the Laboratory
Mouse, 2nd. ed. (Green E. L., ed), pp. 337-350. McGraw-Hill, New
J., Bitensky L., and Chambers M. G. (1996) Modulation of murine osteoarthritis.
Cell Biochemistry and Function 14, 57-61.
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.
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.
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,
E. (1961) Urine specific gravity and osmolality in inbred strains of mice.
J. Appl. Physiol. 16, 194-196.
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,
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.
INBRED STRAINS OF MICE
Updated 9 Apr. 1998
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,