Behavior genetic analysis of Water-T-Maze learning in inbred strains of mice, their hybrids, and selected second generation crosses

1981 ◽  
Vol 43 (3) ◽  
pp. 335-345 ◽  
Author(s):  
H. Schwegler ◽  
W. Buselmaier
1972 ◽  
Vol 55 (2) ◽  
pp. 415-420 ◽  
Author(s):  
B. E. ELEFTHERIOU ◽  
D. W. BAILEY

SUMMARY Plasma corticosterone levels were determined fluorometrically in mice of two unrelated highly inbred strains, C57BL/6By and BALB/cBy, and in seven of their derived recombinant-inbred strains as well as their F1 hybrid and backcross generations necessary to arrive at a genetic model for plasma corticosterone levels. It was concluded that the simplest genetic model, and one which fits the experimental results, was one which assumed that plasma corticosterone levels are controlled genetically by two loci with the epistatic interaction indicating dependency of pathways of action for the two genes.


2008 ◽  
Vol 33 (8) ◽  
pp. 693-707 ◽  
Author(s):  
D. J. Reiner ◽  
T. A. Jan ◽  
J. D. Boughter ◽  
C.-X. Li ◽  
L. Lu ◽  
...  

1998 ◽  
Vol 785 (2) ◽  
pp. 236-244 ◽  
Author(s):  
Lynn A Hyde ◽  
Blair J Hoplight ◽  
Victor H Denenberg

1995 ◽  
Vol 269 (1) ◽  
pp. L6-L10
Author(s):  
M. Takahashi ◽  
S. R. Kleeberger ◽  
T. L. Croxton

Genetic factors influence the responses of humans and rodents to ozone (O3) inhalation. We previously demonstrated differential O3-induced decreases of tracheal potential (VT) in C57BL/6J (B6) and C3H/HeJ (C3) strain mice. To characterize the genetic basis of this strain-specific response, we measured VT in progeny of B6 and C3 strain mice and in six additional inbred strains of mice 6 h after O3 exposures (2 ppm x 3 h). First filial generation (F1) mice and second generation backcrosses with the resistant parent were uniformly resistant. The distribution of VT in second generation backcrosses with the susceptible parent resembled that of a population composed of resistant and susceptible mice in a 1:1 ratio. These data suggested simple autosomal recessive inheritance of susceptibility. However, overlapping distributions prevented statistical confirmation of that hypothesis. Strain screening revealed a susceptible phenotype in 129/J, A/J, B6, C3HeB/FeJ, and SJL/J and a resistant phenotype in AKR/J, C3, and CBA/J inbred mouse strains. Because this pattern of susceptibility to changes in VT differs from that of susceptibility to lung inflammation, the genetic factors that determine these two responses to acute O3 are not identical.


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