Effects of Hypoxia on the Ventral Root Motor-Evoked potential in the In Vitro Spinal Cord Preparation

我们利用体外制剂研究了缺氧对脊髓运动通路突触传递的影响。分离新生大鼠颈脊髓，在室温下灌注含氧人工脑脊液（aCSF）。实验记录了C7腹侧神经根对腹外侧神经束（VLF）刺激的腹侧神经根运动诱发电位（VR-MEP）。VR-MEP分为前期和后期两部分。aCSF中的Ca^<2+>被Mn^<2+>取代，可逆地阻断了支持它们是跨突触起源的两种成分。在缺氧aCSF灌注10-40 min内，VR-MEP中两组分的振幅增加到对照组的130-140%，然后在90 min内逐渐下降到30%。缺氧时早期成分潜伏期延长。60 min复氧后，VR-MEP振幅恢复到80-95%，潜伏期完全恢复。抑制氨基酸拮抗剂士的宁（2muM）和微毒素（1muM）的应用消除了缺氧早期观察到的VR-MEP振幅的增强。结果表明，在缺氧早期，VR-MEP的振幅增加是由于抑制性突触传递的选择性抑制。

We studied the effects of hypoxia on synaptic transmission of motor pathway in spinal cord using in vitro preparations.The cervical spinal cords of neonatal rats were isolated and superfused with oxygenated artificial cerebrospinal fluid (aCSF) at room temperature. The ventral root motor evoked potentials (VR-MEP) were recorded from C7 ventral roots in responce to stimulation to the ventrolateral funiculus (VLF) at Cl.VR-MEP consisted of the early and the late components. The replacement of Ca^<2+> in aCSF by Mn^<2+> reversibly blocked both components supporting them to be trans-synaptic origin. Within 10-40 min of superfusion with hypoxic aCSF,the amplitudes of both components in VR-MEP increased to 130-140% of the control, and then declined progressively to 30% in 90 min. The latency of the early component was prolonged during hypoxia. After 60 min rexygenation, VR-MEP amplitudes recovered to 80-95% with full restoration of the latency.The application of inhibitory amino acid antagonists strychnine (2muM) and picrotoxin (1muM) abolished the augmentation of VR-MEP amplitudes observed in the early phase of hypoxia. The present results suggested that in the early phase of hypoxia amplitudes of VR-MEP were increased because of selective depression of inhibitory synaptic transmission.