of Mice: CBA
Inbr: F90-170 depending on substrain. Agouti. Genet. + . Developed by Strong
in 1920 from a cross of a Bagg albino female and a DBA male. Strain CBA
was selected for a low mammary tumour incidence and C3H for a high incidence.
Now widely distributed, and used as a general-purpose strain. Differences
between substrains are probably too large to be accounted for by mutation,
and some degree of genetic contamination in the past is probable. The
following major substrains are recognised:
CBA/Ca or CBA/H
Strong, to Jackson Laboratory, to Haldane and Gruneberg in 1932. To Carter
1947 and Harwell 1954. This substrain used in most British research.
Jackson Laboratory, to Haldane 1932, to Bonser (Leeds) approx. 1933.
Harwell, to National Institutes of Health in 1966. Carries sex-linked immunological
deficit which prevents it from responding to type III pneumococcal polysaccharide.
Deficit is expressed on B cells (Gershon
and Kondo, 1976
; Scher et al
., 1976). Do not carry naturally
occurring tumour-reactive antibodies commonly found in other strains (Martin and Martin, 1975
Strong, to Andervont 1947, to Jackson Laboratory 1948. Carries gene for
retinal degeneration (rd).
Skin grafts between CBA/J and CBA/Ca
are rejected (Green and Kaufer, 1965
Original strain maintained by Strong.
T6 translocation backcrossed to CBA/H by Dr M. F. Lyon. Now homozygous
for the marker translocation T(14;15) 6Ca, but otherwise congenic with
Low spontaneous bar-pressing activity (13/14), low tail rattling during
aggressive encounters (13/14), high social grooming during aggressive
encounters (2/14), low intrastrain aggression (13/14) (Southwick and Clark, 1966
, 1968). Low locomotor activity
(5/5) (Davis and King, 1967
). Low locomotor
activity when single (6/6), but intermediate when grouped (4/6) (Davis et al., 1967
., 1967). Low spontaneous locomotor activity
(2/9) (Nikulina et al 1991
). Low shock
avoidance learning (9/9) (Bovet et al., 1966
1966, 1969). High shock avoidance learning in Ca substrain (2/8) but not
in J substrain (5/8) (Wahlsten, 1973
water-escape learning in CBA-T6 (2/6) (Festing, 1973b). Highly susceptible
(1/9) to "pinch-induced" catalepsy (excessive freezing), possibly due
to a sinlge recessive autosomal gene (Kulikov
et al, 1993
Life-span and spontaneous disease
Life-span intermediate both sexes (J substrain) in conventional conditions
(11/22 = 527 days males, 10/22 = 527 days females) (Storer,
1966). Life-span (Ca substrain) short in males (4/17 = 486 days) and
long in females (17/17 = 825 days) in SPF fostered conditions. Short life-span
of males associated with a high incidence of haemothorax, suggesting a
high sensitivity to vitamin K deficiency in SPF conditions (Festing and Blackmore, 1971).
High gross tumour incidence (J) (3/22) (Storer, 1966).
Overall tumour incidence 29% in males, 55% in females, including lymphoma
6% in males, 15% in females, hepatoma 24% in males, zero in females and
mammary tumours 33% in females and zero in males (Smith
et al., 1973., 1973). Lung adenomas 2-11% in BrA substrain, leukaemia
4-10% (Muhlbock and Tengbergen, 1971).
Resistant to the induction of atherosclerosis by a high-fat and high-cholesterol
diet (1/13) (Roberts and Thompson, 1976).
Develop a mild hearing loss with onset late in life (contrast C57BL/6J)
(Li, 1992, Willott
et al, 1993, Li et al, 1993, Li and Borg, 1993). Do not carry any of the single recessive
genes found in BALB/cBy, C57BL/6 and WB/ReJ, causing age-related hearing
loss. All three genes are present in DBA/2 (Willott
et al, 1995).
Normal physiology and biochemistry
High systolic blood pressure (4/19) (Schlager
and Weibust, 1967). Low Na/K ratio in erythrocytes (8/9) and in plasma
(9/9) (Waymouth, 1973). High serum ceruloplasmin
levels in males of Ca and J substrains (5/26 and 6/26), high level in
females of Ca substrain (3/27) but intermediate in J substrain (Meier and MacPike, 1968). Low calcium uptake by the heart
(5/5) (Mokler and Iturrian, 1973).
High proportion of the time spent sleeping (2/6), with large percentage
of slow-wave sleep (1/6) and low percentage of paradoxical sleep (5/6)
(Valatx and Bugat, 1974). Low percentage
of paradoxical sleep (7/7) (Pagel et al., 1973.,
1973). Low metabolic rate (14/18) according to Storer (1967),
but high metabolic rate (2/6) according to Pennycuik (1967).
High cell turnover in J substrain as estimated by rapid clearance of DNA-bound
radioactivity (2/17) (Heiniger et al., 1972.,
High peripheral nerve conduction velocity (2/6) (Hegmann,
1972). High brain glutamic acid decarboxylase (3/10) (Gaitonde and Festing, 1976). Low hypoxanthine-guanine phosphoribosyl
transferase in thalamus (6/7), but high level in hypothalamus (2/7) (Suran, 1973). High brain monoamine oxidase (1/7)
and low level of catechol-O-methyltransferase (6/7) activity
(Tunnicliff et al., 1973., 1973).
Low brain tyrosine hydroxylase activity (5/5) (Ciranello et al., 1972., 1972). Low peptidyl proline hydroxylase
activity in mammary gland, foot pad and tumours (5/5) (Cutroneo et al., 1973., 1973). High sensitivity to thyrotropin
in J substrain (1/21) (Levy et al., 1965.,
1965). High coumarin hydroxylating ability (cf. 4/13) (Lush and Arnold, 1975). High hepatic 3 aminolaevulinic
acid synthetase activity after DDC treatment (1/15) (Gross and Hutton, 1971). High porphyrin content in Harderian
gland (3/16) (Margolis, 1971). High hind foot
pad temperature (1/9) (Shepard and Habas,
1967). Have only about 20% of the maltase (gamma-glucoamylase) activity
found in other strains, though there is no evidence for any gross metabolic
abnormality resulting from this defect (Quezada-Calvillo et al, 1993).
Large brain weight (17/18 male, 16/18 female) (Storer,
). Large forebrain volume (2/9) and neocortex (2/9) (Wimer et al., 1969
., 1969). Small brain/body weight ratio
(17/20) (Roderick et al., 1973
Low testes weight (7/8) (Shire and Bartke,
). Large kidney/body weight ratio (5/21) (Schlager,
). Low thyroid weight (4/5) (Mendoza
et al., 1967
., 1967). Small heart/body weight ratio (5/5) (Mokler and Iturrian, 1973
). Large pituitary (2/6) (Sinha et al., 1975
., 1975). Low total leukocyte count (15/18),
high erythrocyte count (6/18) (Russell et
., 1951). Few bristles on foot pads (8/8) (Festing, 1974a).
Third molars small and one or more absent in about 18% of individuals
(Hummel et al., 1966
Resistant to urethane-induced lung tumours (Falconer
and Bloom, 1962
). Susceptible to skin ulceration by DMBA (cf. 13/22)
(Thomas et al., 1973
., 1973). Susceptible
to induction of leukaemia (2/6) and liver tumours (2/6) by neonatally
administered DMBA (Flaks, 1968
to X-irradiation (27/27) (Roderick, 1963
but resistant to `CNS syndrome' with high doses of X-irradiation (1/5)
). Susceptible to hyperbaric oxygen,
showing central nervous system manifestations (11/18) (Hill et al., 1968
., 1968). Sensitive to lethal effect of
ozone (2/21) (Goldstein et al., 1973
1973), but resistant (cf 3/8) to ozone-induced decreases of tracheal potential
(Takahashi et al, 1995
to teratogenic effect of acetazolamide (1/6) (Green
et al., 1973, Hackman and Hurley 1983
1983), but resistant to induction of cleft palate in embryos by cortisone
(5/5) (Kalter, 1965
). Insensitive to insulin
(7/9) (Brown, 1965
). Long survival on Warfarin
(11/12) (Lush and Arnold, 1975
). High ED50
to behavioural effects of nicotine (16/19) (Marks
et al 1989
). Susceptible to weight loss induced by cocaine, but this
is attenuated by anisomycin (cf C3H, SJL) (Shimosato
et al, 1994
). More resistant to acute toxic effects of aflatoxin B-1
than strain C57BL/6 (Almeida et al, 1996
Low lymphocyte phytohaemagglutinin response (35/43) (Heiniger et al., 1975
., 1975). Good immune response to
low doses of bovine gamma-globulin (cf. 4/8) (Levine
and Vaz, 1970
). Good splenic PFC immune response to pneumococcal polysaccharide
in CBA/H-T6 (3/9), but poor in CBA/J (9/9) and CBA/H (7/9) (Amsbaugh et al., 1972
., 1972). Good immune response to
ovomucoid, but poor response to ovalbumin (cf. 5/12) (Vaz et al., 1971
., 1971). Resistant to induction of antigen-induced
arthritis (contrast `most other strains') (Brackertz
et al., 1977
., 1977). Non-responder to synthetic polypeptide Glu57
(cf. 4/7) (Pinchuck
and Maurer, 1965
). Discriminator between `H' and `L' sheep red blood
cells (cf. 12/18) (McCarthy and Dutton,
). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein et al., 1974
., 1974). Low responder to dextran
(cf. 6/10) (Blomberg et al., 1972
1972). Low immune response to ganglio-series gangliosides (c.f. 4/10)
Kawashima et al (1992
). High natural
killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (2/6)
(Pope et al, 1994
). Diminished expression
of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated
T lymphoblasts in J substrain (cf 3/6) (Muthing,
Resistant to infection by Salmonella typhimurium
strain C5 (7/7)
(Plant and Glynn, 1974
). Susceptible to
infection by liver fluke Opisthorchis felineus
). Good plateau harvest of Mycobacterium leprae
after infection (1/9) (Shepard and Habas,
). Low immune response to Mycobacterium lepraemurium
is associated with an impared macrophage function (Saito and Natori 1985
). Resistant to infection by Helicobacter
with only mild gastritis in the antrum and no atrophy seen
over time (cf BALB/c, contrast 4 other strains) (Sakagami et al, 1996
). Resistant to induction of diabetes
mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher et al., 1975
., 1975). Highly susceptible to measles
virus (cf. 3/6) (Rager-Zisman et al.,
., 1976). Ca, H-T6 and N substrains carry no detectable endogenous
ecotropic MuLV DNA sequences (Jenkins et
). Administration of cadmium results in a high incidence of
activation of latent herpes simplex virus infections. This is not seen
in other strains, and does not correlate with cadmium toxicity (Fawl et al, 1996
J substrain resistant (2/7) to the induction of dental caries due to infection
with Streptococcus mutans (Kurihara
et al 1991). Resistant (4/4) to murine herpes virus (Kapoor et al 1992). Resistant to intra-vaginally innoculated
Neisseria gonorrhoeae (c.f. 5/5) (Johnson
et al 1989). Develop severe lesions (2/8) following infection with
Candida albicans (Ashman et al, 1993).
This correlates with low induction of Candida-specific gamma
interferon (Ashman and Bolitho, 1993).
CBA/J resistant, with low amylase response to the fungus Paracoccidioides
brasiliensis (cf 6/12) (Xidieh et al,
J substrain is susceptible to several clinical isolates of penicillin-susceptible
and resistant strains of Streptococcus pneumoniae, and may be
a useful model for evaluating antibiotic efficiencies against this bacterium
(Tateda et al, 1996). Resistant to Leishmania
major (contrast BALB/c) (Laskay et al,
1995). Ca substrain susceptible to L. major mexicana, and
vaccination against the parasite using liposomes with parasite membrane
antigens was effective (cf C57BL/6 but contrast C57BL/10) (Lazama-Davila,
1997). Infection with larval Echinococcus multilocularis by transportal
injection of hyatid homogenate results in well developed protoscoleces
(cf 4/9) (Nakaya et al, 1997).
Good breeding performance (9/25), colony output 1.15 young/female/week,
litter size at weaning 5.8(11/25), T6 substrain about equal (Festing 1976a,
original data). Intermediate breeding performance (4/8), litter size 5.4,
sterility 5.2% (Nagasawa et al., 1973
1973). Good litter size (1/6 to 3/6, depending on parity), but low proportion
of females produce four or more litters (2/6) (Fernandes et al., 1973
., 1973). Poor breeding performance
in N substrain (21/24) (Hansen et al., 1973
1973). Low percentage pre-implantation loss of embryos (2/8) (Leonard et al., 1971
., 1971). Females have a high rate
of fetal resorption when mated with DBA/2 males, but this can be dramatically
reduced by immunization with BALB/c, but not DBA/2J spleen cells. This
may provide an animal model for the prevention of fetal death by vaccination
(Chaouat et al 1985
). Maturity of the
cytoplasm in oocytes is acquired earlier than in those of the KE or other
strains of mice so far studied. (Polanski 1990
Recommended host for transplantable rhabdomyosarcoma BW 10139 (Kaliss,
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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,