背部拉菲到底侧杏仁核皮质皮质otropin释放因子电路调节可卡因-记忆再巩固
Jobe L Ritchie1, Shuyi Qi1, David A Soto1
1Department of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, WA, USA.
概括
寻找可卡因的行为通过抑制底侧杏仁体 (BLA) 中的背脊拉菲核 (DR) 皮质otropin释放因子 (CRF) 神经元来减少. 这突出了一个DR CRF到BLA电路.
科学领域:
- 神经科学是一个神经科学.
- 成研究 研究成研究
- 分子生物学分子生物学
背景情况:
- 环境线索引发可卡因渴望和复发,通过重新激活与毒品相关的记忆.
- 记忆的重新激活可能会破坏记忆的稳定,需要重新巩固以保持持久性.
- 在底侧杏仁体 (BLA) 中的皮质otropin释放因子 (CRF) 信号传递对于可卡因记忆的再巩固至关重要.
研究的目的:
- 为了研究背脊拉菲核 (DR) CRF神经元投射到BLA在可卡因记忆再巩固中的作用.
- 为了确定抑制BLA中的DR CRF神经元是否可以减弱寻找可卡因的行为.
主要方法:
- 训练老鼠自行服用可卡因,并接受灭绝训练.
- 仅由设计药物 (DREADDs) 激活的设计受体在DR CRF神经元中被选择性地表达.
- 可卡因记忆被重新激活,随后是DREADD激动剂或载体的BLA内注射.
- 评估了寻找药物的行为和神经元激活 (c-Fos).
主要成果:
- 在BLA内注入DREADD激动剂德洛克洛zapine (DCZ) 显著降低了在记忆重新激活后寻找可卡因的行为.
- 这种效应是特定于表达DREADD的老鼠,并且取决于记忆的重新激活.
- 投射到BLA的DR CRF神经元在记忆再巩固过程中表现出增加的活动 (c-Fos) 和共同表达的膀性谷氨酸运输体3.
结论:
- DR CRF → BLA 电路参与维持可卡因在不稳定后的记忆强度.
- 抑制这种电路减弱了寻找可卡因的行为,这表明了治疗目标.
- 在BLA中释放的DR CRF和/或谷氨酸可能会调解可卡因记忆的再巩固.
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