McBrayer Zofeyah L, Dimova Jiva, Pisansky Marc T, Sun Mu, Beppu Hideyuki, Gewirtz Jonathan C, O'Connor Michael B
Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
Department of Psychology and Neuroscience, University of Minnesota, Minneapolis, Minnesota, United States of America.
PLoS One. 2015 Oct 7;10(10):e0139860. doi: 10.1371/journal.pone.0139860. eCollection 2015.
To investigate the role of Bone Morphogenic Protein Receptor Type II (BMPRII) in learning, memory, and exploratory behavior in mice, a tissue-specific knockout of BMPRII in the post-natal hippocampus and forebrain was generated. We found that BMPRII mutant mice had normal spatial learning and memory in the Morris water maze, but showed significantly reduced swimming speeds with increased floating behavior. Further analysis using the Porsolt Swim Test to investigate behavioral despair did not reveal any differences in immobility between mutants and controls. In the Elevated Plus Maze, BMPRII mutants and Smad4 mutants showed reduced anxiety, while in exploratory tests, BMPRII mutants showed more interest in object exploration. These results suggest that loss of BMPRII in the mouse hippocampus and forebrain does not disrupt spatial learning and memory encoding, but instead impacts exploratory and anxiety-related behaviors.
为了研究骨形态发生蛋白II型受体（BMPRII）在小鼠学习、记忆和探索行为中的作用，我们构建了出生后海马体和前脑BMPRII组织特异性敲除的小鼠模型。我们发现，BMPRII突变小鼠在莫里斯水迷宫中的空间学习和记忆能力正常，但游泳速度显著降低，漂浮行为增加。使用波索尔特游泳试验进一步分析行为绝望情况，未发现突变体与对照组在不动时间上有任何差异。在高架十字迷宫中，BMPRII突变体和Smad4突变体表现出焦虑减轻，而在探索试验中，BMPRII突变体对物体探索表现出更大兴趣。这些结果表明，小鼠海马体和前脑中BMPRII的缺失不会破坏空间学习和记忆编码，而是会影响探索行为和与焦虑相关的行为。
