Choosing the best genetic strains of mice for developing a new knockout or transgenic mouse requires extensive knowledge of the endogenous traits of inbred strains. Background genes from the parental strains may interact with the mutated gene, in a manner which could severely compromise the interpretation of the mutant phenotype. The present overview summarizes the literature on a wide variety of behavioral traits for the 129, C57BL/6, DBA/2, and many other inbred strains of mice. Strain distributions are described for open field activity, learning and memory tasks, aggression, sexual and parental behaviors, acoustic startle and prepulse inhibition, and the behavioral actions of ethanol, nicotine, cocaine, opiates, antipsychotics, and anxiolytics. Using the referenced information, molecular geneticists can choose optimal parental strains of mice, and perhaps develop new embryonic stem cell progenitors, for new knockouts and transgenics to investigate gene function, and to serve as animal models in the development of novel therapeutics for human genetic diseases.

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It has been suggested that the Y chromosome of DBA/1Bg mice makes an incremental contribution to their aggressive behavior and to that of the C57BL/10 female X DBA/1 male F1 hybrids. To test this hypothesis, a congenic stock of C57BL/10 with the DBA/1 Y chromosome was developed by the backcross system of breeding; the stock is designated C57BL/10-Y1. There were no significant differences in aggressive behavior between the congenic C57BL/10 and C57BL/10-Y1. However, the hybrid B10D1 F1 and D1B10-Y1 F1 had identical aggression scores, and both of these were more aggressive than the hybrid D1B10 F1. These findings support the hypothesis that there is an interaction between DBA/1 Y chromosomes and autosomes in the development of intermale aggression of these mice.

It is well established that the agonistic behavior of offense in mice is heritable. However, few genes have been identified or mapped for offense. For segments of chromosomes with effects on offense, a positional candidate strategy can be used to find such genes. This approach is illustrated for the effect of the male specific part (nonpseudoautosomal region; NPAR) of the mouse Y chromosome on offense. It is proposed that a positional candidate for this effect is Sry. The Sry protein is a transcription factor. Its mRNA is expressed in fetal and adult brain. Its protein binds to response elements in the 5' end of the aromatase and the Fra1 genes. Each of these genes has potential effects on several brain neurotransmitter systems involved in offense. The NPAR Y chromosomes of several pairs of inbred strains have differential effects on offense. This hypothesis would be tested by sequencing Sry for some of these pairs of strains.

Indications of a role for the nonpseudoautosomal region of the Y chromosome (YNPAR) in intermale attack behavior have been demonstrated by Maxson's group using C57BL/10 (B10) and DBA/1 (D1) inbred mouse strains and their reciprocal congenics. Carlier and Roubertoux' group, using CBA/H (H) and NZB/B1NJ (N) mice, did not find such a YNPAR effect. For the two research groups, however, not only were the parental strains different, but also the rearing conditions and testing methods. The divergent conclusions drawn may therefore have been due either to genetic variation or to environment-related variables. We carried out two experiments to investigate these alternatives. The N and H strains were raised and tested according to the experimental design used by Maxson's group (homogeneous set test) and the D1 and B10 strains were raised and tested according to the experimental design of Carlier and Roubertoux' group (standard opponent test). Considering all studies together, the YNPAR effect appeared in both sets of mice only when using the homogeneous set test. This raises the question of what environmentally related variables are involved in the YNPAR effect on intermale attack. One strong hypothesis is that the different types of opponents in each experimental design send differing olfactory signals, which, in turn, differentially affect the capacity to elicit intermale attack behavior.