从小鼠的电路屏幕上，该课题组发现了一组在睡眠剥夺（SD）期间激活的丘脑核胞连（RE）神经元，这些神经元是睡眠稳态所必需的。光遗传学激活的RE神经元导致了一种非遗传表型：睡眠前行为（梳理和筑巢），随后是类似RS的长时间高强度睡眠。在SD期间抑制RE活动会损害随后的RS，这表明这些神经元发出睡眠需要的信号。RE神经元在促进睡眠的无色带细胞的上游活动，SD触发该回路的可塑性以加强它们的连通性。这些发现揭示了一种回路机制，通过这种机制，睡眠需求改变了睡眠回路的功能耦合，从而促进了持久的深度睡眠。
据悉，长时间的清醒导致持续的深度恢复性睡眠（RS）。然而，介导这一过程的神经元回路仍然处于休眠状态。
附：英文原文
Title: Sleep need–dependent plasticity of a thalamic circuit promotes homeostatic recovery sleep
Author: Sang Soo Lee, Qiang Liu, Alexandra H. R. Cheng, Dong Won Kim, Daphne M. Boudreau, Anuradha Mehta, Mehmet F. Keles, Rafal Fejfer, Isabelle Palmer, Kristen H. Park, Heike Münzberg, Timothy D. Harris, Austin R. Graves, Seth Blackshaw, Mark N. Wu
Issue&Volume: 2025-06-19
Abstract: Prolonged wakefulness leads to persistent, deep recovery sleep (RS). However, the neuronal circuits that mediate this process remain elusive. From a circuit screen in mice, we identified a group of thalamic nucleus reuniens (RE) neurons activated during sleep deprivation (SD) and required for sleep homeostasis. Optogenetic activation of RE neurons leads to an unusual phenotype: presleep behaviors (grooming and nest organizing) followed by prolonged, intense sleep that resembles RS. Inhibiting RE activity during SD impairs subsequent RS, which suggests that these neurons signal sleep need. RE neurons act upstream of sleep-promoting zona incerta cells, and SD triggers plasticity of this circuit to strengthen their connectivity. These findings reveal a circuit mechanism by which sleep need transforms the functional coupling of a sleep circuit to promote persistent, deep sleep.
DOI: adm8203
Source: https://www.science.org/doi/10.1126/science.adm8203