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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >NPAS2 as a transcriptional regulator of non-rapid eye movement sleep: Genotype and sex interactions
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NPAS2 as a transcriptional regulator of non-rapid eye movement sleep: Genotype and sex interactions

机译：NPAS2作为非快速眼动睡眠的转录调节因子：基因型和性别相互作用

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摘要

Because the transcription factor neuronal Per-Arnt-Sim-type signal-sensor protein-domain protein 2 (NPAS2) acts both as a sensor and an effector of intracellular energy balance, and because sleep is thought to correct an energy imbalance incurred during waking, we examined NPAS2's role in sleep homeostasis using npas2 knockout (npas2(-/-)) mice. We found that, under conditions of increased sleep need, i.e., at the end of the active period or after sleep deprivation (SD), NPAS2 allows for sleep to occur at times when mice are normally awake. Lack of npas2 affected electroencephalogram activity of thalamocortical origin; during non-rapid eye movement sleep (NREMS), activity in the spindle range (10-15 Hz) was reduced, and within the delta range (1-4 Hz), activity shifted toward faster frequencies. In addition, the increase in the cortical expression of the NPAS2 target gene period2 (pert) after SD was attenuated in npas2(-/-) mice. This implies that NPAS2 importantly contributes to the previously documented wake-dependent increase in cortical per2 expression. The data also revealed numerous sex differences in sleep; in females, sleep need accumulated at a slower rate, and REMS loss was not recovered after SD. In contrast, the rebound in NREMS time after SD was compromised only in npas2(-/-) males. We conclude that NPAS2 plays a role in sleep homeostasis, most likely at the level of the thalamus and cortex, where NPAS2 is abundantly expressed.
机译：由于转录因子神经元Per-Arnt-Sim型信号传感器蛋白结构域蛋白2（NPAS2）既可以充当细胞内能量平衡的传感器又可以发挥作用，并且由于睡眠被认为可以纠正醒来时产生的能量不平衡，我们使用npas2基因敲除（npas2（-/-））小鼠研究了NPAS2在睡眠稳态中的作用。我们发现，在睡眠需求增加的条件下，即在活动期结束时或在睡眠剥夺（SD）后，NPAS2可使小鼠在正常清醒时发生睡眠。 npas2缺乏影响丘脑皮层来源的脑电图活动；在非快速眼动睡眠（NREMS）中，纺锤体范围（10-15 Hz）的活动减少，而在增量范围（1-4 Hz）中，活动向更快的频率转移。另外，在npas2（-/-）小鼠中，SD后NPAS2靶基因period2（pert）皮质表达的增加被减弱。这意味着NPAS2对先前记录的皮层per2表达的依赖尾迹的增加起重要作用。数据还显示，睡眠中存在许多性别差异。在女性中，睡眠需求以较慢的速度积累，SD后仍未恢复REMS丧失。相反，SD后的NREMS时间反弹仅在npas2（-/-）雄性中受到影响。我们得出结论，NPAS2在睡眠稳态中发挥作用，最有可能在丘脑和皮质水平表达NPAS2丰富。

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