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药物强化通过抑制状胆固醇神经元来降低认知灵活性,从而损害了认知灵活性
Himanshu Gangal1,2, Xueyi Xie1, Zhenbo Huang1
1Department of Neuroscience and Experimental Therapeutics, School of Medicine, Texas A&M University Health Science Center, Bryan, TX, 77807, USA.
Nature communications
|June 30, 2023
概括
药物使用通过加强特定脑细胞 (dMSNs) 之间的连接来破坏认知灵活性,这些细胞抑制其他细胞 (CINs),这对于灵活的行为至关重要. 这个电路解释了成如何损害目标导向的行动.
科学领域:
- 神经科学是一个神经科学.
- 成研究 研究成研究
- 认知科学 认知科学
背景情况:
- 药物使用障碍与认知灵活性受损有关.
- 这些缺陷背后的神经机制仍然不完全理解.
- 状回路,特别是涉及中等脊状神经元 (MSN) 和胆能内神经元 (CIN),涉及到奖励处理和认知控制.
研究的目的:
- 调查假设,通过物质使用诱导的条状直通路MSNs (dMSNs) 的活性增加会抑制CIN,从而降低认知灵活性.
- 阐明特定的神经回路调解强化诱导的认知灵活性缺陷.
主要方法:
- 可卡因管理的动物模型.
- 电生理学记录以评估突触传输和神经元激发.
- 化学遗传和光遗传技术来操纵神经元活动.
- 狂犬病媒介病毒追踪用于电路映射.
- 工具反向学习任务来测量认知灵活性.
主要成果:
- 暴露于可卡因诱导的长期强化阻断性传播从dMSN到CIN在背中条体 (DMS).
- 使用物质降低了DMS CIN发射率.
- 通过化学遗传学或光遗传学抑制DMS CINs损害了目标导向行为灵活性.
- 已知介导强化的SNR投射的dMSN被发现可以抑制DMS CINs.
结论:
- 在DMS中,从dMSN到CIN的局部抑制电路调解强化诱导的认知灵活性缺陷.
- 针对这种dMSN-CIN通路可能为与成相关的认知障碍提供治疗策略.
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