Mileykovskiy Boris Y, Kiyashchenko Lyudmila I, Siegel Jerome M
Veterans Administration, Greater Los Angeles Health System, Sepulveda, California, USA.
J Physiol. 2002 Dec 15;545(3):997-1006. doi: 10.1113/jphysiol.2002.028985.
The pontine oral reticular nucleus, gigantocellular reticular nucleus (Gi) and dorsal paragigantocellular nucleus (DPGi) of the medulla are key elements of a brainstem-reticulospinal inhibitory system that participates in rapid eye movement (REM) sleep atonia. Our recent study has shown that excitation of these brainstem nuclei in decerebrate rats inhibits locus coeruleus cells and the midbrain locomotor region neurons related to muscle tone facilitation. In the present study we have examined the influences of electrical and chemical stimulation of Gi and DPGi inhibitory sites on the activity of neurons located in the magnocellular part of the red nucleus (RMC), a cell group that participates in both the tonic and phasic regulation of motor output. A total of 192 RMC neurons were recorded in precollicular-premammillary decerebrate rats with muscle rigidity and induced locomotion. Thirty-three RMC neurons were identified antidromically as rubrospinal (RMC-spinal) cells by stimulation of the contralateral dorsolateral funiculus at the L2 level. A total of 141 RMC neurons (88.7 %) and all RMC-spinal neurons were inhibited during electrical stimulation of Gi and DPGi inhibitory sites. This cessation of activity was correlated with bilateral muscle atonia or blockage of locomotion. Six RMC cells (3.8 %) were excited (224 +/- 50 %, n = 6, minimum = 98, maximum = 410, P < 0.05) and 11 cells (7 %) gave no response to Gi and DPGi stimulation. Microinjections of kainic acid (100 microM, 0.2 microl) into Gi and DPGi inhibitory sites, previously identified by electrical stimulation, produced a short-latency (35 +/- 3.5 s, n = 11) decrease of rigid hindlimb muscle tone and inhibition of all tested RMC (n = 7) and RMC-spinal (n = 5) neurons. These results, combined with our recent published data, suggest that inhibition of motor function during activation of the brainstem inhibitory system is related to both the descending inhibition of spinal motoneurons and suppression of activity in supraspinal motor facilitatory systems. These two mechanisms acting synergistically may cause generalized motor inhibition during REM sleep and cataplexy.
脑桥嘴侧网状核、延髓巨细胞网状核（Gi）和背侧旁巨细胞网状核（DPGi）是脑干网状脊髓抑制系统的关键组成部分，该系统参与快速眼动（REM）睡眠期的肌张力缺失。我们最近的研究表明，在去大脑大鼠中，刺激这些脑干核会抑制蓝斑细胞以及与肌张力促进相关的中脑运动区神经元。在本研究中，我们检测了电刺激和化学刺激Gi和DPGi抑制位点对红核大细胞部（RMC）神经元活动的影响，RMC是一个参与运动输出的紧张性和位相性调节的细胞群。在具有肌肉强直和诱发性运动的中脑前 - 乳头前区去大脑大鼠中，共记录了192个RMC神经元。通过在L2水平刺激对侧背外侧索，逆向鉴定出33个RMC神经元为红核脊髓（RMC - 脊髓）细胞。在电刺激Gi和DPGi抑制位点期间，总共141个RMC神经元（88.7%）以及所有RMC - 脊髓神经元均受到抑制。这种活动停止与双侧肌肉张力缺失或运动阻断相关。6个RMC细胞（3.8%）被兴奋（224±50%，n = 6；最小值 = 98，最大值 = 410，P < 0.05），11个细胞（7%）对Gi和DPGi刺激无反应。向先前通过电刺激确定的Gi和DPGi抑制位点微量注射谷氨酸（100 μM，0.2 μl），导致后肢强直肌张力出现短潜伏期（35±3.5 s，n = 11）降低，并抑制了所有测试的RMC（n = 7）和RMC - 脊髓（n = 5）神经元。这些结果与我们最近发表的数据相结合，表明在脑干抑制系统激活期间运动功能的抑制与脊髓运动神经元的下行抑制以及脊髓上运动促进系统活动的抑制均有关。这两种机制协同作用可能导致REM睡眠和猝倒期间的全身性运动抑制。
