Genetic reduction of noradrenergic function alters social memory and reduces aggression in mice

Abstract

Aberrant social behavior is a hallmark of many cognitive, mood, and neurological disorders, although the specific molecular mechanisms underlying the behavioral deficits are not well understood. The neurotransmitter noradrenaline (NA) has been implicated in some of these disorders, as well as in several aspects of social behavior in humans and animals. We tested dopamine β-hydroxylase knockout ( Dbh −/−) mice that lack NA in various social behavior paradigms. Dbh −/− mice have relatively normal performance in the elevated plus maze, light/dark box, and open field test – three measures of anxiety – and a social recognition test. In contrast, Dbh −/− mice displayed a specific deficit in a social discrimination task and had a nearly complete absence of resident-intruder aggression. These results indicate that intact NA signaling is required for some types of social memory and aggression, but that a lack of NA does not greatly affect anxiety in mice. Further exploration of NA deficits in neurological disease may reveal mechanisms of aberrant social behavior.