巩固过程中多巴胺活动的短暂变化通过睡眠中断损害长期记忆。

Lin Yan, Litao Wu, Timothy D Wiggin, Xiaojuan Su, Wei Yan, Hailiang Li, Lei Li, Zhonghua Lu, Yuantao Li, Zhiqiang Meng, Fang Guo, Fan Li, Leslie C Griffith, Chang Liu
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引用次数: 0

摘要

睡眠障碍与较差的长期记忆(LTM)形成有关,但相关的潜在细胞类型和神经回路尚未完全解码。多巴胺神经元(DANs)参与多个阶段的记忆处理。本研究表明,在记忆巩固的最初几个小时内,原大脑前内侧神经元(PAM-DANs)的短暂激活或一对后内侧背神经元(DPM)的抑制会损害24小时的LTM。有趣的是,睡眠剥夺会提高PAM-DANs和DPM神经元的神经活动,而PAM-DANs的短暂热激活或DPM神经元的失活会导致睡眠缺失和碎片化。这种手法后的睡眠药物恢复LTM。PAM- dans的一个特定子集,PAM-α1,与DPM神经元突触连接,指定连接睡眠和记忆的微电路。PAM- dans,包括PAM-α1,主要通过Dop1R1受体与DPM神经元形成功能性突触,抑制DPM。我们的数据表明,PAM(-α1)-DPM微电路的训练后活动,特别是在记忆巩固期间,在维持LTM巩固所需的睡眠中起着至关重要的作用,为睡眠与记忆之间的复杂关系提供了新的细胞和电路基础。
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Brief disruption of activity in a subset of dopaminergic neurons during consolidation impairs long-term memory by fragmenting sleep.

Sleep disturbances are associated with poor long-term memory (LTM) formation, yet the underlying cell types and neural circuits involved have not been fully decoded. Dopamine neurons (DANs) are involved in memory processing at multiple stages. Here, using both male and female flies, Drosophila melanogaster , we show that, during the first few hours of memory consolidation, disruption of basal activity of a small subset of protocerebral anterior medial DANs (PAM-DANs), by either brief activation or inhibition of the two dorsal posterior medial (DPM) neurons, impairs 24 h LTM. Interestingly, these brief changes in activity using female flies result in sleep loss and fragmentation, especially at night. Pharmacological rescue of sleep after manipulation restores LTM. A specific subset of PAM-DANs (PAM-α1) that synapse onto DPM neurons specify the microcircuit that links sleep and memory. PAM-DANs, including PAM-α1, form functional synapses onto DPM mainly via multiple dopamine receptor subtypes. This PAM-α1 to DPM microcircuit exhibits a synchronized, transient, post-training increase in activity during the critical memory consolidation window, suggesting an effect of this microcircuit on maintaining the sleep necessary for LTM consolidation. Our results provide a new cellular and circuit basis for the complex relationship between sleep and memory.

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