Maze learning and effects of pretraining in inbred strains of mice.

1962 ◽  
Vol 55 (5) ◽  
pp. 748-752 ◽  
Author(s):  
Gardner Lindzey ◽  
Harvey Winston
Keyword(s):  
Inbred Strains ◽  
Maze Learning ◽  
Inbred Strains Of Mice

Water version of the radial-arm maze: Learning in three inbred strains of mice

1998 ◽  
Vol 785 (2) ◽  
pp. 236-244 ◽  
Author(s):  
Lynn A Hyde ◽  
Blair J Hoplight ◽  
Victor H Denenberg
Keyword(s):  
Inbred Strains ◽  
Maze Learning ◽  
Radial Arm Maze ◽  
Inbred Strains Of Mice

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

Duplications and deletions of Vh genes in inbred strains of mice

1988 ◽  
Vol 28 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Adele Tutte ◽  
Roy Riblet
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Vh Genes

scholarly journals THE GENETIC DIVERGENCE OF SUBLINES AS ASSESSED BY HISTOCOMPATIBILITY TESTING

Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 671-677
Author(s):  
Willys K Silvers ◽  
David L Gasser
Keyword(s):  
Genetic Divergence ◽  
Inbred Strains ◽  
Skin Grafts ◽  
Inbred Strains Of Mice ◽  
Inbred Rats

ABSTRACT The degree of genetic divergence which has occurred between a number of inbred strains of mice and between two sublines of inbred rats was assessed by determining the fate of inter-subline skin grafts. Sublines which had been separated for 29 and 42 generations possessed no detectable incompatibility, while three combinations of sublines judged to have been maintained apart for from 123 to 129 generations showed slight degrees of histoincompatibility. One pair of sublines which had been separated for 119 generations demonstrated a marked degree of incompatibility, and an F2 test suggested that mutations had occurred at four or five histocompatibility loci.

scholarly journals A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.

1990 ◽  
Vol 171 (2) ◽  
pp. 519-531 ◽  
Author(s):  
A Matsuzawa ◽  
T Moriyama ◽  
T Kaneko ◽  
M Tanaka ◽  
M Kimura ◽  
...  
Keyword(s):  
Recessive Gene ◽  
Mutant Gene ◽  
Inbred Strains ◽  
Lymphoid Hyperplasia ◽  
Lymphoid Cells ◽  
Autoantibody Production ◽  
Genetic Studies ◽  
Inbred Strains Of Mice ◽  
Backcross Populations ◽  
Generalized Lymphadenopathy

Several mice with generalized lymphadenopathy were found in the CBA/KlJms (CBA) colony maintained at our institute. A new mutant strain of mice that develop massive lymphoid hyperplasia at 100% incidence within 5 mo after birth was established by crossing these diseased mice. Genetic studies on lymphadenopathy were conducted in F1, F2, and backcross populations from crosses between mutant CBA (CBA-m) and various inbred strains of mice. The results supported the control of lymphadenopathy by a single autosomal recessive gene. Since C3H/He-gld/gld (C3H-gld), MRL/MpJ-lpr/lpr (MRL-lpr), and C3H/HeJ-lpr/lpr (C3H-lpr) mice develop the same type of lymphoid hyperplasia, allelism of the mutant gene with gld or lpr was tested by investigating lymphadenopathy in F1 and backcross populations from crosses between CBA-m and C3H-gld, MRL-lpr, or C3H-lpr mice. The gene was confirmed to be allelic with lpr but not with gld. Interestingly, however, the mutant gene interacted with gld to induce less severe lymphadenopathy. Thus, the mutant gene was named lprcg, an lpr gene complementing gld in induction of lymphoproliferation. The genetic conclusion was supported by the same profile of surface markers of lymphoid cells with gld/gld, lpr/lpr, lprcg/lprcg, lprcg/lpr, and +/gld +/lprcg genotypes, as well as by massive lymph node hyperplasia and high titers of autoantibodies in the first four genotypes, but slight hyperplasia and insignificant autoantibody production in the last. The discovery of lprcg provided strong genetic evidence for the parallels between anomalous phenotypes of gld and lpr, and CBA/KlJms-lprcg/lprcg mice will contribute to elucidation of the mechanism of induction of the same abnormal differentiation and functions of lymphocytes by gld and lpr.

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