PDF(Pubmed)
Abstract：
Rapid eye movement sleep (REMs) is characterized by activated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams. REMs is homeostatically regulated, ensuring that any loss of REMs is compensated by a subsequent increase in its amount. However, the neural mechanisms underlying the homeostatic control of REMs are largely unknown. Here, we show that GABAergic neurons in the preoptic area of the hypothalamus projecting to the tuberomammillary nucleus (POAGAD2→TMN neurons) are crucial for the homeostatic regulation of REMs in mice. POAGAD2→TMN neurons are most active during REMs, and inhibiting them specifically decreases REMs. REMs restriction leads to an increased number and amplitude of calcium transients in POAGAD2→TMN neurons, reflecting the accumulation of REMs pressure. Inhibiting POAGAD2→TMN neurons during REMs restriction blocked the subsequent rebound of REMs. Our findings reveal a hypothalamic circuit whose activity mirrors the buildup of homeostatic REMs pressure during restriction and that is required for the ensuing rebound in REMs.
摘要：
快速眼动睡眠（REM）的特征是激活的脑电图（EEG）和肌肉无力，伴随着生动的梦。REM是稳态调节的，确保REM的任何损失由随后的金额增加来补偿。然而,REM稳态控制的神经机制在很大程度上是未知的。这里,我们表明，下丘脑视前区的GABA能神经元（POAGAD2→TMN神经元）对小鼠REM的稳态调节至关重要。POAGAD2→TMN神经元在REM期间最活跃，并抑制它们特异性地减少REM。REM限制导致POAGAD2→TMN神经元中钙瞬变的数量和幅度增加，反映了REM压力的积累。在REM限制过程中抑制POAGAD2→TMN神经元会阻止随后的REM反弹。我们的发现揭示了下丘脑回路，其活动反映了限制过程中稳态REM压力的积累，这是随后REM反弹所必需的。
