| First Author | Kawashita E | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 5 | Pages | e97947 |
| PubMed ID | 24874880 | Mgi Jnum | J:216521 |
| Mgi Id | MGI:5608943 | Doi | 10.1371/journal.pone.0097947 |
| Citation | Kawashita E, et al. (2014) Altered behavior in mice with deletion of the alpha2-antiplasmin gene. PLoS One 9(5):e97947 |
| abstractText | BACKGROUND: The alpha2-antiplasmin (alpha2AP) protein is known to be a principal physiological inhibitor of plasmin, and is expressed in various part of the brain, including the hippocampus, cortex, hypothalamus and cerebellum, thus suggesting a potential role for alpha2AP in brain functions. However, the involvement of alpha2AP in brain functions is currently unclear. OBJECTIVES: The goal of this study was to investigate the effects of the deletion of the alpha2AP gene on the behavior of mice. METHODS: The motor function was examined by the wire hang test and rotarod test. To evaluate the cognitive function, a repeated rotarod test, Y-maze test, Morris water maze test, passive or shuttle avoidance test and fear conditioning test were performed. An open field test, dark/light transition test or tail suspension test was performed to determine the involvement of alpha2AP in anxiety or depression-like behavior. RESULTS AND CONCLUSIONS: The alpha2AP knockout (alpha2AP-/-) mice exhibited impaired motor function compared with alpha2AP+/+ mice. The alpha2AP-/- mice also exhibited impairments in motor learning, working memory, spatial memory and fear conditioning memory. Furthermore, the deletion of alpha2AP induced anxiety-like behavior, and caused an anti-depression-like effect in tail suspension. Therefore, our findings suggest that alpha2AP is a crucial mediator of motor function, cognitive function, anxiety-like behavior and depression-like behavior, providing new insights into the role of alpha2AP in the brain functions. |
