Chen J R, Tseng G F
Department of Anatomy, College of Medicine, National Taiwan University, Taipei.
Neuroscience. 1997 Jul;79(2):449-62. doi: 10.1016/s0306-4522(96)00704-x.
Membrane properties and inhibitory synaptic connections of normal and axotomized rat rubrospinal neurons were examined using a coronal slice preparation. Rubrospinal neurons were axotomized at the C2 vertebral level in vivo. Retrograde labelling in vivo and intracellular biocytin injection following recording were combined to identify recorded axotomized rubrospinal neurons. Their input resistances decreased three and four days and became higher than normal four and 10 weeks following lesioning which coincided with a sequential increase and decrease of their soma area. On the other hand, although their membrane time-constant was reduced three and four days following lesioning, it returned to normal value four and 10 weeks following axotomy. Other than these, their membrane current-voltage relationship including an inward rectification in the hyperpolarizing direction was not altered. Normal rubrospinal neurons generated very fast spikes which were not affected by axotomy. Both normal and axotomized cells generated trains of repetitive spikes with a fast spike frequency adaptation at the beginning upon suprathreshold current injection. However, the slope of the steady-state spike frequency and applied current relationship was increased four and 10 weeks following axotomy which also showed an increased steady-state spike frequency in response to high-amplitude current injection. Synaptically, the amplitude and duration of the monosynaptic inhibitory potential evoked from nearby reticular formation were reduced following axotomy. In addition, fewer rubrospinal neurons were found to receive this inhibition 10 weeks following axotomy. Thus, our results show that spinal axotomy induces a time-dependent modification of the membrane properties and spike generating behaviour of rubrospinal neurons which probably represents an initial decrease and a later increase of their excitability. This is accompanied by a persistent decrease of synaptic inhibition which is expected to affect structures that remained innervated by the undamaged axon collaterals of these spinally axotomized neurons.
采用冠状切片标本，研究了正常和轴突切断大鼠红核脊髓神经元的膜特性及抑制性突触连接。在体内C2椎体水平切断红核脊髓神经元的轴突。结合体内逆行标记和记录后细胞内生物素注射，以识别记录的轴突切断的红核脊髓神经元。损伤后3天和4天，它们的输入电阻降低，损伤后4周和10周高于正常水平，这与它们的胞体面积的相继增加和减少相一致。另一方面，虽然损伤后3天和4天它们的膜时间常数降低，但轴突切断后4周和10周又恢复到正常值。除此之外，它们的膜电流-电压关系，包括超极化方向的内向整流，没有改变。正常的红核脊髓神经元产生非常快速的动作电位，不受轴突切断的影响。正常和轴突切断的细胞在阈上电流注入开始时都产生一连串重复的动作电位，且动作电位频率快速适应。然而，轴突切断后4周和10周，稳态动作电位频率与施加电流关系的斜率增加，这也表明在高幅度电流注入时稳态动作电位频率增加。在突触方面，轴突切断后，从附近网状结构诱发的单突触抑制电位的幅度和持续时间减小。此外，轴突切断后10周，发现接受这种抑制的红核脊髓神经元较少。因此，我们的结果表明，脊髓轴突切断诱导红核脊髓神经元膜特性和动作电位产生行为的时间依赖性改变，这可能代表其兴奋性最初降低和随后升高。这伴随着突触抑制的持续降低，预计会影响这些脊髓轴突切断神经元未受损轴突侧支仍支配的结构。
