Takakusaki K, Kohyama J, Matsuyama K, Mori S
Department of Physiology II, Asahikawa Medical College, Japan.
Exp Brain Res. 1993;93(3):471-82. doi: 10.1007/BF00229362.
Intrapontine microinjections of serotonin in acutely decerebrated cats resulted in the bilateral augmentation of the postural muscle tone of the hindlimbs. Optimal injection sites were located in the dorsomedial part of the rostral pontine reticular formation corresponding to the nucleus reticularis pontis oralis (NRPo). In this study, attempts were made to elucidate the cellular basis for the serotoninergically induced augmentation of postural muscle tone by recording the electromyographic (EMG) activity of hindlimb extensor muscles, the monosynaptic reflex responses evoked by electrical stimulation of group Ia muscle afferent fibres and the membrane potentials of hindlimb alpha-motoneurons (MNs). Serotonin injections resulted not only in the augmentation of the EMG activity of gastrocnemius soleus muscles, but also in the restoration of EMG suppression, which was induced by previous injection of carbachol into the NRPo. Extensor and flexor monosynaptic reflex responses were facilitated by serotonin injections into the NRPo. Such reflex facilitation was not induced by serotonin injections into the mesencephalic or the medullary reticular formation. Intrapontine serotonin injections resulted in membrane depolarization of extensor and flexor MNs with decreases in input resistance and rheobase. Spontaneous depolarizing synaptic potentials (EPSPs) increased in both frequency and amplitude. Peak voltage of Ia monosynaptic EPSPs also increased. Serotonin injections which followed carbachol injections resulted in membrane depolarization of MNs along with an increase in the frequency of spontaneous EPSPs and a decrease in carbachol-induced inhibitory postsynaptic potentials. Following pontine carbachol injections, antidromic and orthodromic responses in MNs were suppressed. Discharges of MNs evoked by intracellular current injections were also suppressed, but were restored following serotonin injections. These results indicate that postsynaptic excitation, presynaptic facilitation and disinhibition (withdrawal of postsynaptic inhibition) simultaneously act on the hindlimb MNs during serotonin-induced postural augmentation and restoration.
在急性去大脑猫脑桥内微量注射5-羟色胺,导致后肢姿势性肌张力双侧增强。最佳注射部位位于脑桥嘴侧网状结构的背内侧部分,对应脑桥嘴侧网状核(NRPo)。在本研究中,通过记录后肢伸肌的肌电图(EMG)活动、电刺激Ia类肌传入纤维诱发的单突触反射反应以及后肢α运动神经元(MNs)的膜电位,试图阐明5-羟色胺能诱导姿势性肌张力增强的细胞基础。5-羟色胺注射不仅导致比目鱼肌腓肠肌的EMG活动增强,还导致先前向NRPo注射卡巴胆碱所诱导的EMG抑制恢复。向NRPo注射5-羟色胺可促进伸肌和屈肌的单突触反射反应。向中脑或延髓网状结构注射5-羟色胺不会诱导这种反射促进作用。脑桥内注射5-羟色胺导致伸肌和屈肌MNs膜去极化,输入电阻和基强度降低。自发性去极化突触后电位(EPSPs)的频率和幅度均增加。Ia单突触EPSPs的峰值电压也增加。在注射卡巴胆碱后注射5-羟色胺导致MNs膜去极化,同时自发性EPSPs频率增加,卡巴胆碱诱导的抑制性突触后电位降低。在脑桥注射卡巴胆碱后,MNs的逆向和顺向反应受到抑制。细胞内电流注射诱发的MNs放电也受到抑制,但在注射5-羟色胺后恢复。这些结果表明,在5-羟色胺诱导的姿势增强和恢复过程中,突触后兴奋、突触前促进和去抑制(突触后抑制的撤除)同时作用于后肢MNs。