Deletion of the prion gene Prnp affects offensive aggression in mice

被引:5
作者
Buedefeld, Tomaz [1 ]
Majer, Aljaz [1 ]
Jerin, Ales [2 ]
Majdic, Gregor [1 ,3 ]
机构
[1] Univ Ljubljana, Fac Vet, Ctr Anim Genom, SI-1000 Ljubljana, Slovenia
[2] Univ Med Ctr Ljubljana, Inst Clin Chem & Biochem, Ljubljana, Slovenia
[3] Univ Maribor, Sch Med, Inst Physiol, SLO-2000 Maribor, Slovenia
关键词
Prnp knockout mouse; Brain; Prion protein; Offensive aggression; Testosterone; DEVELOPMENTAL EXPRESSION; SYNAPTIC PLASTICITY; MOLECULAR-BIOLOGY; MESSENGER-RNA; PROTEIN; SCRAPIE; BEHAVIOR; SEROTONIN; DISEASE; BRAIN;
D O I
10.1016/j.bbr.2014.03.006
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:216 / 221
页数:6
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