Miyata Y, Yasuda H
Department of Pharmacology, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
Neurosci Res. 1988 Apr;5(4):338-46. doi: 10.1016/0168-0102(88)90035-1.
Monosynaptic excitatory postsynaptic potentials (EPSPs) were recorded from the triceps surae motoneurons in the rat. Two to 3 weeks after section of the medial gastrocnemius (MG) nerve, Ia EPSPs evoked by stimulation of the MG nerve were significantly depressed, as reported previously. However, the MG EPSP amplitude significantly increased within 24 h, reaching a maximum on the 3rd day after axotomy. This increase was prevented by actinomycin-D treatment, indicating that the synaptic enhancement is dependent upon protein synthesis. When disuse of sensory fibers was induced without injuring the muscle nerve, the degree of synaptic enhancement was similar to that after axotomy. Therefore, the enhancement of central synaptic transmission shortly after axotomy is due to the loss of electrical activity, but not due to the axon reaction of the Ia sensory neurons to injury. It is postulated that the presence of some factor in Ia sensory fibers enhances synaptic transmission, while electrical activity of the neurons antagonizes the action of this factor.
在大鼠的腓肠肌运动神经元中记录单突触兴奋性突触后电位(EPSP)。如先前报道,切断腓肠肌内侧头(MG)神经2至3周后,刺激MG神经诱发的Ia类EPSP显著降低。然而,MG EPSP的幅度在24小时内显著增加,在轴突切断术后第3天达到最大值。放线菌素-D处理可阻止这种增加,表明突触增强依赖于蛋白质合成。当在不损伤肌神经的情况下诱导感觉纤维废用时,突触增强程度与轴突切断术后相似。因此,轴突切断后不久中枢突触传递的增强是由于电活动的丧失,而不是由于Ia类感觉神经元对损伤的轴突反应。据推测,Ia类感觉纤维中某种因子的存在增强了突触传递,而神经元的电活动则拮抗该因子的作用。