Open AccessAltered Behavior in Mice with Deletion of the Alpha2-Antiplasmin Gene
Author(s) -
Eri Kawashita,
Yosuke Kanno,
K. Ikeda,
Hiromi Kuretake,
Osamu Matsuo,
Hiroyuki Matsuno
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0097947
Subject(s) - tail suspension test , morris water navigation task , open field , rotarod performance test , behavioural despair test , neuroscience , hippocampus , fear conditioning , psychology , knockout mouse , motor coordination , elevated plus maze , anxiety , biology , amygdala , endocrinology , psychiatry , motor activity , genetics , gene , antidepressant
Background The α2-antiplasmin (α2AP) 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 α2AP in brain functions. However, the involvement of α2AP in brain functions is currently unclear. Objectives The goal of this study was to investigate the effects of the deletion of the α2AP 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 α2AP in anxiety or depression-like behavior. Results and Conclusions The α2AP knockout (α2AP −/− ) mice exhibited impaired motor function compared with α2AP +/+ mice. The α2AP −/− mice also exhibited impairments in motor learning, working memory, spatial memory and fear conditioning memory. Furthermore, the deletion of α2AP induced anxiety-like behavior, and caused an anti-depression-like effect in tail suspension. Therefore, our findings suggest that α2AP is a crucial mediator of motor function, cognitive function, anxiety-like behavior and depression-like behavior, providing new insights into the role of α2AP in the brain functions.