Variation in pentobarbitone sleeping time in mice 2. Variables affecting test results

1986 ◽  
Vol 20 (2) ◽  
pp. 91-96 ◽  
Author(s):  
D. P. Lovell
Keyword(s):  
Environmental Factors ◽  
Total Variation ◽  
Small Proportion ◽  
Inbred Strains ◽  
Laboratory Animals ◽  
Test Results ◽  
Sleeping Time ◽  
Inbred Strains Of Mice ◽  
Baseline Values ◽  
Pentobarbitone Sleeping Time

The effect of some environmental factors on the pentobarbitone sleeping time (PST) in inbred strains of mice has been investigated. Age, dose level and fasting before the test significantly altered the PST while the source of the drug and regular handling of the mice had no effect. None of these factors affected strains differentially. Unsystematic effects such as litter differences contributed only a small proportion of the total variation in the experiments. The strain rankings were different from those obtained in some previous experiments. The effects of some of the environmental factors on the PST did not always agree with previous work. The implications of these results for the design of similar experiments and the relevance of baseline values in laboratory animals are discussed.

Variation in pentobarbitone sleeping time in mice 1. Strain and sex differences

1986 ◽  
Vol 20 (2) ◽  
pp. 85-90 ◽  
Author(s):  
D. P. Lovell
Keyword(s):  
Sex Differences ◽  
Environmental Factors ◽  
Strain Differences ◽  
Inbred Strains ◽  
Genetic Differences ◽  
Strain Variation ◽  
Sleeping Time ◽  
Inbred Strains Of Mice ◽  
Designed Experiment ◽  
Pentobarbitone Sleeping Time

A set of 23 inbred strains of mice was tested for their sleeping time under sodium pentobarbitone anaesthetic. Highly significant strain differences were found. Estimates of the proportion of the variation accounted for by genetic differences ranged from 28% to 42%. In general, males slept longer than females but the size of the sex differences was not consistent across strains. Sleeping times on different test days also varied, indicating that environmental factors were affecting the results. A specially designed experiment failed to detect any differences in within-strain variation.

Variation in barbiturate sleeping time in mice 3. Strain × environment interactions

1986 ◽  
Vol 20 (4) ◽  
pp. 307-312 ◽  
Author(s):  
D. P. Lovell
Keyword(s):  
Environmental Factors ◽  
Inbred Strains ◽  
Bedding Material ◽  
Sleeping Time ◽  
Pharmacological Response ◽  
Materials Used ◽  
Bedding Materials ◽  
Over Time ◽  
Pentobarbitone Sleeping Time

Environmental factors such as diet, bedding material and temperature at the time of testing affected a 'model' pharmacological response - pentobarbitone sleeping time - differentially in a range of inbred strains. These results are probably explained by variations in the responses of the strains to constituents of the diets and bedding materials used in the experiments. Differences in the results between experiments suggest that there are also fluctuations in the composition of the diets and bedding materials over time. Strain × environment interactions such as those found here may explain differences in strain rankings between experiments. They would also account for some of the variability in results found between laboratories and within a laboratory over time.

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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