In the previous sections, we have shown that individual differences in behavior can be partly explained by genetic variation. Obviously, genetic variation is not the only source of variation; differences in the environment also play an important role. This section focuses on the border of both sources of variation—the so-called gene-environment interaction. Generally, the term refers to the phenomenon that the behavioral expression of the genotype depends on the environment.
A recent example of a gene-environment interaction in aggression research is a study that compared the behavior of male mice in which the brain-specific isoform of the creatine kinase gene was knocked out with animals that did not lack the gene (wild types). Both knockouts and wild types were tested for their aggressive behavior in the neutral cage paradigm. In this test the encounters took place on neutral grounds;
that is, neither the animal under investigation nor its opponent were familiar with the test cage. Moreover, each mouse was tested twice on consecutive days against genetically different standard opponents. At first, knockouts did not seem to differ from wild types: Both were similarly aggressive against whichever opponent. A more detailed analysis, however, revealed that knockouts were more prone to attack one of the two opponents, whereas wild types showed no preferences.
Another example showing that the behavioral expression of the genotype depends on the environment comes from mice that lack a specific part of the NMDA receptor in a specific section of their hippocampus. As mentioned previously, when raised under normal laboratory conditions, they perform relatively poorly in learning and memory tasks. However, when they are exposed to an enriched environment each day for an extended period, they improve markedly and do as well as normal mice in various tasks. This behavioral enhancement is reflected anatomically: The number of connections between hippocampal cells actually increases. Hence, in these mice the enriched environment counterbalances a genetically engineered memory defect.
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