大脑皮层中的DCC对于小鼠的认知功能是必需的
Yun-Qing Hu1, Wei-Tang Liu1,2, Yong Wu3
1State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Brain pathology (Zurich, Switzerland)
|September 18, 2024
概括
在结直肠癌 (DCC) 中被删除的基因与精神分裂症 (SZ) 有关. 在小鼠的大脑特定区域的DCC缺乏导致记忆和感官门缺陷,这些缺陷被抗精神病药物逆转.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 遗传学 是一个
- 精神病学是一个精神病学.
背景情况:
- 精神分裂症 (SZ) 是高度遗传的,与被删除的结直肠癌 (DCC) 基因有遗传联系.
- 以前的研究表明,SZ患者的大脑中的DCC表达减少.
研究的目的:
- 调查DCC在SZ病原发生中的作用.
- 识别与SZ相关的新型DCC单核酸多态 (SNPs) 相关的SZ.
- 在小鼠中探索DCC缺乏的行为和分子后果.
主要方法:
- 产生的DCC条件淘汰赛 (CKO) 小鼠,在皮层V和VI的向删除.
- 评估行为表型,包括恐惧记忆,空间记忆和感觉运动门 (预脉冲抑制测试).
- 分析了分子变化,包括蛋白质水平 (p-AKT,p-GSK3α/β),神经元脊柱密度和大脑振荡.
主要成果:
- 在皮质层VI中删除DCC,但不删除层V,损害恐惧/空间记忆和感觉运动门.
- 在缺乏DCC的小鼠中,olanzapine治疗恢复了感觉运动门.
- 在缺乏DCC的小鼠中观察到降低的p-AKT和p-GSK3α/β水平,降低了金字塔神经元脊柱密度,以及乱的三角振荡.
结论:
- DCC是精神分裂症的风险基因,其缺乏可以促进类似于SZ的表型.
- 涉及AKT和GSK3α/β的下游信号通路与DCC相关的SZ病原发生有关.
- 这些发现为精神分裂症背后的分子机制提供了新的见解.
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