Havton L, Kellerth J O
Department of Anatomy, University of Umeå, Sweden.
Exp Brain Res. 1990;79(1):75-82. doi: 10.1007/BF00228874.
Chronic axotomy of a peripheral motor nerve in cat causes a gradual reduction in the number of intramedullary axon collaterals originating from the axotomized motoneurons (Havton and Kellerth 1984, 1989). This axon collateral elimination would be expected to reduce the amount of recurrent inhibitory reflex actions mediated by these cells. The aim of the present study was to investigate the recurrent inhibition originating from axotomized motoneurons and, also, to see whether the elimination of axon collaterals from the axotomized neurons might induce secondary compensatory changes in the recurrent inhibitory pathways originating from synergistic non-lesioned motoneurons. The results, which were obtained by means of intracellular recordings and monosynaptic reflex testing, indicate that postoperative enhancement of reflex actions may take place in the recurrent inhibitory pathways persisting in the axotomized motoneurons as well as in those originating from synergistic nonlesioned motoneurons. It is suggested that the site of compensatory enhancement is at the synaptic reflex contacts between the motoraxon collaterals and the inhibitory Renshaw interneurons.
切断猫的外周运动神经会导致其慢性轴突切断，使得源自轴突切断的运动神经元的髓内轴突侧支数量逐渐减少（哈夫顿和凯勒思，1984年、1989年）。预计这种轴突侧支的消除会减少由这些细胞介导的反复抑制性反射活动的量。本研究的目的是研究源自轴突切断的运动神经元的反复抑制，同时观察从轴突切断的神经元消除轴突侧支是否可能在源自协同作用的未受损运动神经元的反复抑制途径中诱导继发性代偿性变化。通过细胞内记录和单突触反射测试获得的结果表明，在轴突切断的运动神经元以及源自协同作用的未受损运动神经元的反复抑制途径中，反射活动的术后增强可能会发生。有人认为，代偿性增强的部位是运动轴突侧支与抑制性闰绍中间神经元之间的突触反射接触点。
