Department of Neurology and Division of Sleep Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Sleep Med. 2013 Aug;14(8):707-13. doi: 10.1016/j.sleep.2013.03.017. Epub 2013 Jun 13.
Rapid eye movement (REM) sleep in mammals is associated with wakelike cortical and hippocampal activation and concurrent postural muscle atonia. Research during the past 5 decades has revealed the details of the neural circuitry regulating REM sleep and muscle atonia during this state. REM-active glutamatergic neurons in the sublaterodorsal nucleus (SLD) of the dorsal pons are critical for generation for REM sleep atonia. Descending projections from SLD glutamatergic neurons activate inhibitory premotor neurons in the ventromedial medulla (VMM) and in the spinal cord to antagonize the glutamatergic supraspinal inputs on the motor neurons during REM sleep. REM sleep behavior disorder (RBD) consists of simple behaviors (i.e., twitching, jerking) and complex behaviors (i.e., defensive behavior, talking). Animal research has lead to the hypothesis that complex behaviors in RBD are due to SLD pathology, while simple behaviors of RBD may be due to less severe SLD pathology or dysfunction of the VMM, ventral pons, or spinal cord.
快速眼动 (REM) 睡眠在哺乳动物中与类似清醒的皮质和海马激活以及同时的姿势肌肉弛缓有关。在过去的 50 年中，研究揭示了调节 REM 睡眠和肌肉弛缓的神经回路的细节。背侧脑桥的 sublaterodorsal 核 (SLD) 中的 REM 活性谷氨酸能神经元对于 REM 睡眠弛缓的产生至关重要。来自 SLD 谷氨酸能神经元的下行投射激活腹内侧 medulla (VMM) 和脊髓中的抑制性运动前神经元，以在 REM 睡眠期间拮抗运动神经元上的谷氨酸能上位输入。REM 睡眠行为障碍 (RBD) 包括简单行为（即抽搐、抽搐）和复杂行为（即防御行为、说话）。动物研究提出假设，即 RBD 的复杂行为是由于 SLD 病变引起的，而 RBD 的简单行为可能是由于 SLD 病变较轻或 VMM、腹侧脑桥或脊髓的功能障碍引起的。
