Deletion of the prion gene Prnp affects offensive aggression in mice

Prion protein (Prp(c)) is involved in the etiology of prion neurodegenerative diseases in mammals. The biological functions of Prp(c) are still largely unknown despite many studies in recent years. Different studies have shown impairment in locomotion, emotional/social behaviors, sleep disorders and memory impairment in mice lacking the prion gene Prnp (Prnp(-/-)) but its exact functions in the brain are still unclear. In the present study, Zurich I Prnp(-/-) and their littermate wild type (WT) control male mice were behaviorally characterized for offensive aggressive behavior in a resident-intruder paradigm with the aim to establish the possible function of Prp(c) in the regulation of offensive aggressive behavior. Prnp(-/-) mice showed reduced latencies to the first attack and bite, higher percentage of mice biting and higher frequencies of attacks of stimulus males. These results show that Prnp(-/-) mice exhibit altered aggressive behavior in comparison to their WT controls and therefore suggest that lack of the Prnp either directly or indirectly affects brain circuitry responsible for the regulation of offensive aggressive behavior.