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在Sapap3-突变小鼠中,皮层-状突触缺陷和强迫症类行为
Jeffrey M Welch1, Jing Lu, Ramona M Rodriguiz
1Department of Neurobiology, Center for Translational Neuroscience, Duke University Medical Center, Durham, North Carolina 27710, USA.
Nature
|August 24, 2007
概括
缺乏SAPAP3蛋白质的小鼠表现出焦虑和强迫性理,类似于强迫症 (OCD). 在条纹体中恢复SAPAP3可以逆转这些强迫症类型的行为,突出其在大脑电路中的作用.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 是一个遗传学.
- 精神病学是一个精神病学.
背景情况:
- 强迫症和强迫症 (OCD) 与皮质 - 条状 - 甲状腺 - 皮质电路功能障碍有关.
- 强迫症背后的确切病原机制仍然不清楚.
- SAP90/PSD95相关蛋白3 (SAPAP3) 是条形体中一个关键的突触后支架蛋白.
研究的目的:
- 调查SAPAP3在皮层-状回路中的作用及其在强迫症类行为中的潜在参与.
- 探索针对强迫症患者SAPAP3的治疗潜力.
主要方法:
- 在小鼠中遗传删除Sapap3以创建模型.
- 行为分析包括焦虑和强迫性理测试.
- 皮质-状突触的电生理学,结构和生物化学评估.
- 通过在状体中使用lentiviral介导的Sapap3表达的救援实验.
主要成果:
- Sapap3-突变小鼠表现出增加的焦虑和强迫性理,导致身体损伤.
- 这些行为通过选择性血清素再吸收抑制剂得到改善.
- 在Sapap3-突变小鼠中发现了皮层-状突触的缺陷.
- 在条纹体中恢复Sapap3可以挽救突触和行为异常.
结论:
- SAPAP3在皮层-状突触中发挥着至关重要的作用.
- 皮质-状回路对于调节与强迫症相关的行为至关重要.
- SAPAP3是强迫症和相关疾病的潜在治疗标.
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