鼠类中枢前额叶皮层中围神经网络改变海马前额叶振荡,重塑可卡因自我管理的记忆
Jereme C Wingert1, Jonathan D Ramos1, Sebastian X Reynolds1
1R.S. Dow Neurobiology, Legacy Research Institute, Portland, Oregon 97232.
概括
在中部前额叶皮层中进行的ABCondroitinase治疗通过改变parvalbumin内部神经元来破坏可卡因自我管理的记忆. 这种效应被新的检索会加强,提供了减少可卡因复发的潜在策略.
科学领域:
- 神经科学是一个神经科学.
- 神经生物学 神经生物学 神经生物学
- 成研究 研究成研究
背景情况:
- 中间前额皮层 (mPFC) 对于可卡因复发至关重要.
- 在mPFC中表达帕瓦胺 (PV) 的内神经元调节其输出.
- 围神经网络覆盖了许多PV内部神经元,影响了它们的可塑性.
研究的目的:
- 为了研究氏丁酶ABC (ABC) 在破坏可卡因自我管理记忆中的有效性.
- 为了确定ABC治疗是否会影响记忆再巩固,特别是可卡因相关行为.
- 探索ABC对记忆再巩固的影响背后的神经机制.
主要方法:
- 在雄性大鼠的mPFC中注入了ABC酶.
- 利用可卡因自我管理模式来建立记忆.
- 通过新的和熟悉的背景进行了检索会话.
- 在mPFC和背部海马体 (dHIP) 中进行了体内电生理学记录.
主要成果:
- ABC治疗减弱了可卡因自我管理的记忆巩固和阻断了再巩固.
- 再巩固封锁只发生在新的检索会话中,而不是熟悉的.
- ABC治疗特别影响了可卡因记忆,而不是糖糖记忆.
- 在原始老鼠中,ABC改变了光伏强度和神经元发射.
- 在新的检索过程中,ABC防止了奖励相关的高频振荡和dHIP-mPFC同步的增加.
结论:
- 当与新的检索会话相结合时,ABCondroitinase会破坏可卡因自我管理记忆的再巩固.
- 这种干扰与神经活动的改变和mPFC和dHIP之间的同步有关.
- 这些发现表明,通过针对记忆再巩固来减少可卡因复发的潜在治疗策略.
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