Takakusaki K, Shimoda N, Matsuyama K, Mori S
Department of Physiology, Asahikawa Medical College, Japan.
Exp Brain Res. 1994;99(3):361-74. doi: 10.1007/BF00228973.
The present study was aimed at elucidating the pontomedullary and spinal cord mechanisms of postural atonia induced by microinjection of carbachol and restored by microinjections of serotonin or atropine sulfate into the nucleus reticularis pontis oralis (NRPo). Medullary reticulospinal neurons (n = 132) antidromically activated by stimulating the L1 spinal cord segment were recorded extracellularly. Seventy-eight of them were orthodromically activated with mono- or disynaptic latencies by stimulating the NRPo area at the site where carbachol injections effectively induced postural atonia. Most of these reticulospinal neurons (71 of 78) were located in the nucleus reticularis gigantocellularis (NRGc). Following carbachol injection into the NRPo, discharge rates of the NRGc reticulospinal neurons (29 of 34) increased, while the activity of soleus muscles decreased bilaterally. Serotonin or atropine injections into the same NRPo area resulted in a decrease in the discharge rates of the reticulospinal neurons with a concomitant increase in the levels of hindlimb muscle tone. Membrane potentials of hindlimb extensor and flexor alpha motoneurons (MNs) were hyperpolarized and depolarized by carbachol and serotonin or atropine injections, respectively. In all pairs of reticulospinal neurons and MNs (n = 11), there was a high correlation between the increase in the discharge rates and the degree of membrane hyperpolarization of the MNs. Spike-triggered averaging during carbachol-induced atonia revealed that inhibitory postsynaptic potentials (IPSPs) were evoked in 15 MNs by the discharges of nine reticulospinal neurons. Four of them evoked IPSPs in more than one MN. The mean segmental delay and the mean time to the peak of IPSPs were 1.6 ms and 2.0 ms, respectively. Axonal trajectories of reticulospinal neurons (n = 6), which evoked IPSPs in MNs, were investigated in the lumbosacral segments (L1-S1) by antidromic threshold mapping. The stem axons descended through the ventral (n = 2) and ventrolateral (n = 4) funiculi in the lumbar segments. All axons projected their collaterals to the intermediate region (laminae V, VI) and ventromedial part (laminae VII, VIII) of the gray matter. All these results suggest that the reticulospinal pathway originating from the NRGc is involved in postural atonia induced by pontine microinjection of carbachol, and that the pathway is inactivated during the postural restoration induced by subsequent injections of serotonin or atropine. It is further suggested that the pontine inhibitory effect is mediated via segmental inhibitory interneurons projecting to MNs.
本研究旨在阐明向口侧脑桥网状核（NRPo）微量注射卡巴胆碱所诱导并经微量注射5-羟色胺或硫酸阿托品恢复的姿势性肌张力缺失的脑桥延髓和脊髓机制。细胞外记录经刺激L1脊髓节段逆向激活的延髓网状脊髓神经元（n = 132）。其中78个神经元在向有效诱导姿势性肌张力缺失的部位注射卡巴胆碱时，经单突触或双突触潜伏期被正向激活。这些网状脊髓神经元大多（78个中的71个）位于巨细胞网状核（NRGc）。向NRPo注射卡巴胆碱后，NRGc网状脊髓神经元（34个中的29个）的放电率增加，而双侧比目鱼肌的活动减少。向同一NRPo区域注射5-羟色胺或阿托品导致网状脊髓神经元放电率降低，同时后肢肌张力水平升高。向延髓后肢伸肌和屈肌α运动神经元（MNs）分别注射卡巴胆碱和5-羟色胺或阿托品后，其膜电位分别出现超极化和去极化。在所有网状脊髓神经元和MNs对（n = 11）中，放电率的增加与MNs膜超极化程度之间存在高度相关性。在卡巴胆碱诱导的肌张力缺失期间进行的触发尖峰平均显示，9个网状脊髓神经元的放电在15个MNs中诱发了抑制性突触后电位（IPSPs）。其中4个在不止一个MNs中诱发了IPSPs。IPSPs的平均节段延迟和平均峰值时间分别为1.6 ms和2.0 ms。通过逆向阈值映射在腰骶段（L1-S1）研究了在MNs中诱发IPSPs的网状脊髓神经元（n = 6）的轴突轨迹。主干轴突在腰段通过腹侧（n = 2）和腹外侧（n = 4）索下行。所有轴突都将其侧支投射到灰质的中间区域（V层、VI层）和腹内侧部分（VII层、VIII层）。所有这些结果表明，起源于NRGc的网状脊髓通路参与了脑桥微量注射卡巴胆碱所诱导的姿势性肌张力缺失，并且该通路在随后注射5-羟色胺或阿托品所诱导的姿势恢复过程中失活。进一步表明，脑桥抑制作用是通过投射到MNs的节段性抑制性中间神经元介导的。
