A developmental-genetic analysis of aggressive behavior in mice: IV. Genotype-environment interaction

To assess the extent of plasticity in behavioral development after directional selection for aggressive behavior, male mice were reared and tested in selected social rearing and testing conditions. After four generations of selective breeding, the lines differed in all attack measures when tested in a dyadic assessment following isolation rearing. Line-specific effects of isolation vs. group rearing were demonstrated, and longitudinal studies showed the ontogenetic pattern of difference between lines to be substantially changed by conditions of rearing and testing. The social-interactional processes that might produce the developmental genotype-environment interaction were investigated. Line-specific interaction patterns within long-established sibling groups predicted aggressive behavior in cross-situational dyadic assessments. Group rearing attenuated most line differences in aggressive measures, but the high-aggressive line was more likely than the low-aggressive line to persist in attacking over consecutive days of observation. Cross-fostering in early development did not significantly change adult aggressive behavior. Some implications of a developmental-genetic approach to the study of social interactions are discussed.     

Dementia praecox as a failure of neoteny

The theory of neoteny assumes that adult animals that are higher on the phylogenetic scale retain juvenile characteristics for greater periods of their lifetime. This hypothesis would account for the continuation of curiosity, learning and playfulness in humans and other higher primates in contrast to less evolved mammals. The failure of the neoteny process could result in humans that have lost these juvenile characteristics and lack motivation, curiosity and the capacity to learn freely. These features are indicative of the negative symptoms of dementia praecox, a chronic mental illness that strikes individuals as they become adults.It is postulated that a possible mechanism in the etiology of dementia praecox is the failure of regulator genes to program structural genes to produce enzymes necessary for neoteny. Positive symptoms of the disorder may be conceptualized as the organisms aberrant response to this activation failure. The role of regulator genes in chronic illness may prove a significant avenue for further investigation.