Basal Forebrain Parvalbumin Neurons Mediate Arousals from Sleep Induced by Hypercarbia or Auditory Stimuli.
Basal Forebrain Parvalbumin Neurons Mediate Arousals from Sleep Induced by Hypercarbia or Auditory Stimuli.
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DOI：
10.1016/j.cub.2020.04.029
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发表时间：
2020-06-22
期刊：
影响因子：
--
通讯作者：
Basheer R
中科院分区：
文献类型：
--
作者：
McKenna JT;Thankachan S;Uygun DS;Shukla C;McNally JM;Schiffino FL;Cordeira J;Katsuki F;Zant JC;Gamble MC;Deisseroth K;McCarley RW;Brown RE;Strecker RE;Basheer R
快速从睡眠中唤醒的能力对生存很重要。然而，睡眠呼吸暂停和其他疾病患者的觉醒增加会阻碍安宁睡眠，并导致认知、代谢和生理功能障碍。目前对哪些神经系统调节这些短暂的觉醒知之甚少，这阻碍了恢复正常睡眠的治疗方法的发展。基底前脑(BF)接受上升觉醒系统的许多核团的输入，包括脑干臂旁神经元，这些神经元促进觉醒，以应对血液中二氧化碳水平的升高，如睡眠呼吸暂停。BF臂旁神经元终末的光抑制损害了皮质对高碳酸血症的觉醒，但哪种类型的BF细胞介导了对高碳酸血症或其他感觉刺激的皮质觉醒尚不清楚。在这里，我们使用光遗传学技术测试了BF小白蛋白(PV)神经元在觉醒中的作用。光刺激BF-PV神经元产生从非快眼运动(NREM)睡眠到觉醒的快速转换，但不影响REM-觉醒转换。与以前对BF谷氨酸和胆碱能神经元的研究不同，刺激BF-PV神经元引起的觉醒很短暂，总觉醒时间仅略有增加，这让人想起睡眠呼吸暂停的临床表现。双侧视觉抑制BF-PV神经元增加了高碳酸血症或听觉刺激引起的觉醒潜伏期。因此，BF-PV神经元是大脑回路的重要组成部分，该回路在睡眠中产生短暂的觉醒，以响应可能表明生理功能障碍或对机体构成危险的刺激。睡眠中短暂的唤醒、呼吸暂停和其他障碍阻碍了睡眠的恢复效果。利用小鼠的光遗传技术，McKenna等人。确认基底前脑小白蛋白神经元是二氧化碳水平升高或声音刺激引起的睡眠短暂唤醒的重要因素。
The ability to rapidly arouse from sleep is important for survival. However, increased arousals in patients with sleep apnea and other disorders prevent restful sleep, and contribute to cognitive, metabolic and physiologic dysfunction. Little is currently known about which neural systems mediate these brief arousals, hindering the development of treatments which restore normal sleep. The basal forebrain (BF) receives inputs from many nuclei of the ascending arousal system including the brainstem parabrachial neurons which promote arousal in response to elevated blood carbon dioxide levels, as seen in sleep apnea. Optical inhibition of the terminals of parabrachial neurons in the BF impairs cortical arousals to hypercarbia, but which BF cell types mediate cortical arousals in response to hypercarbia or other sensory stimuli is unknown. Here we tested the role of BF parvalbumin (PV) neurons in arousal using optogenetic techniques in mice. Optical stimulation of BF-PV neurons produced rapid transitions to wakefulness from non-rapid-eye movement (NREM) sleep but did not affect REM-wakefulness transitions. Unlike previous studies of BF glutamatergic and cholinergic neurons, arousals induced by stimulation of BF-PV neurons were brief and only slightly increased total wake time, reminiscent of clinical findings in sleep apnea. Bilateral optical inhibition of BF-PV neurons increased the latency to arousal produced by exposure to hypercarbia or auditory stimuli. Thus, BF-PV neurons are an important component of the brain circuitry which generates brief arousals from sleep in response to stimuli which may indicate physiological dysfunction or danger to the organism. Brief arousals from sleep in sleep apnea and other disorders hinder the restorative effects of sleep. Using optogenetic techniques in mice, McKenna et al. identify basal forebrain parvalbumin neurons as an important contributor to brief arousals from sleep elicited by increased carbon dioxide levels or acoustic stimuli.
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DOI：
10.1073/pnas.1202526109
发表时间：
2012-09-25
影响因子：
11.1
作者：
Carter, Matthew E.;Brill, Julia;de Lecea, Luis
通讯作者：
de Lecea, Luis
影响因子：
16.6
作者：
Anaclet C;Pedersen NP;Ferrari LL;Venner A;Bass CE;Arrigoni E;Fuller PM
通讯作者：
Fuller PM
影响因子：
2
作者：
Dringenberg, Hans C.;Sparling, Joseph S.;Murdoch, Jennifer
通讯作者：
Murdoch, Jennifer
影响因子：
2.5
作者：
McKenna, James T.;Yang, Chun;Franciosi, Serena;Winston, Stuart;Abarr, Kathleen K.;Rigby, Matthew S.;Yanagawa, Yuchio;McCarley, Robert W.;Brown, Ritchie E.
通讯作者：
Brown, Ritchie E.
影响因子：
2.5
作者：
Duque, A;Balatoni, B;Zaborszky, L
通讯作者：
Zaborszky, L