BDNF‐restricted knockout mice as an animal model for aggression

• Published in: Genes, brain and behavior brain and behavior, 2011-04, Vol.10 (3), p.365-374
• Main Authors: Ito, W., Chehab, M., Thakur, S., Li, J., Morozov, A.
• Format: Article
• Language: English
• Subjects: Aggression; Aggression - physiology; animal model; Animals; BDNF; Behavior; Brain; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - deficiency; Brain-Derived Neurotrophic Factor - genetics; Cre recombinase; Disease Models, Animal; Female; Genetic Predisposition to Disease - genetics; knockout; Male; Maze Learning - physiology; Mental Disorders - genetics; Mental Disorders - physiopathology; Mental Disorders - psychology; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Social Behavior
• ISSN: 1601-1848; 1601-183X
• DOI: 10.1111/j.1601-183X.2010.00676.x

Mice with global deletion of one brain‐derived neurotrophic factor (BDNF) allele or with forebrain‐restricted deletion of both alleles show elevated aggression, but this phenotype is accompanied by other behavioral changes, including increases in anxiety and deficits in cognition. Here we performed behavioral characterization of conditional BDNF knockout mice generated using a Cre recombinase driver line, KA1‐Cre, which expresses Cre in few areas of brain: highly at hippocampal area CA3 and moderately in dentate gyrus, cerebellum and facial nerve nucleus. The mutant animals exhibited elevated conspecific aggression and social dominance, but did not show changes in anxiety‐like behaviors assessed using the elevated plus maze and open field test. There were no changes in depression‐like behaviors tested in the forced swim test, but small increase in immobility in the tail suspension test. In cognitive tasks, mutants showed normal social recognition and normal spatial and fear memory, but exhibited a deficit in object recognition. Thus, this knockout can serve as a robust model for BDNF‐dependent aggression and object recognition deficiency.