The Mina and Everard Goodman Faculty of Life Sciences and The Leslie and Susan Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, 5290002, Ramat Gan, Israel.
Center for Sleep Sciences and Medicine, Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA, 94305, USA.
Mol Neurobiol. 2017 Oct;54(8):6581-6597. doi: 10.1007/s12035-016-0175-x. Epub 2016 Oct 12.
Sleep is tightly regulated by the circadian clock and homeostatic mechanisms. Although the sleep/wake cycle is known to be associated with structural and physiological synaptic changes that benefit the brain, the function of sleep is still debated. The hypothalamic hypocretin/orexin (Hcrt) neurons regulate various functions including feeding, reward, sleep, and wake. Continuous imaging of single neuronal circuits in live animals is vital to understanding the role of sleep in regulating synaptic dynamics, and the transparency of the zebrafish model enables time-lapse imaging of single synapses during both day and night. Here, we use the gephyrin (Gphnb) protein, a central inhibitory synapse organizer, as a fluorescent post-synaptic marker of inhibitory synapses. Double labeling showed that Gphnb-tagRFP and collybistin-EGFP clusters co-localized in dendritic inhibitory synapses. Using a transgenic hcrt:Gphnb-EGFP zebrafish, we showed that the number of inhibitory synapses in the dendrites of Hcrt neurons was increased during development. To determine the effect of sleep on the inhibitory synapses, we performed two-photon live imaging of Gphnb-EGFP in Hcrt neurons during day and night, under light/dark and constant light and dark conditions, and following sleep deprivation (SD). We found that synapse number increased during the night under light/dark conditions but that these changes were eliminated under constant light or dark conditions. SD reduced synapse number during the night, and the number increased during post-deprivation daytime sleep rebound. These results suggest that rhythmic structural plasticity of inhibitory synapses in Hcrt dendrites is independent of the circadian clock and is modulated by consolidated wake and sleep.
睡眠受到昼夜节律钟和内稳态机制的严格调节。虽然睡眠/觉醒周期与有益于大脑的结构和生理突触变化有关,但睡眠的功能仍存在争议。下丘脑食欲肽/食欲素(Hcrt)神经元调节各种功能,包括进食、奖励、睡眠和觉醒。在活体内对单个神经元回路进行连续成像对于理解睡眠在调节突触动力学中的作用至关重要,并且斑马鱼模型的透明性使得能够在白天和黑夜对单个突触进行延时成像。在这里,我们使用 Gephyrin(Gphnb)蛋白作为抑制性突触的荧光后突触标记物,来研究单个突触。双标记显示 Gphnb-tagRFP 和 collybistin-EGFP 簇在树突抑制性突触中共同定位。使用 hcrt:Gphnb-EGFP 转基因斑马鱼,我们发现 Hcrt 神经元树突中的抑制性突触数量在发育过程中增加。为了确定睡眠对抑制性突触的影响,我们在光/暗和恒光/暗条件下以及睡眠剥夺(SD)后,对 Hcrt 神经元中的 Gphnb-EGFP 进行了双光子活体成像。我们发现,在光/暗条件下,夜间突触数量增加,但在恒光或恒暗条件下,这些变化被消除。SD 在夜间减少了突触数量,而在剥夺后白天的睡眠反弹中,突触数量增加。这些结果表明,Hcrt 树突中抑制性突触的节律性结构可塑性独立于昼夜节律钟,并受巩固的清醒和睡眠调节。