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

采用离体培养的新生大鼠颈髓，在室温下用含氧人工脑脊液（aCSF）灌流，观察缺氧对脊髓运动通路突触传递的影响。在C1刺激腹外侧索（VLF）时，从C7前根记录到前根运动诱发电位（VR-MEP），VR-MEP包括早、晚两个成分。Mn^2+取代aCSF中的Ca^2+可逆地阻断了这两种成分，支持它们是跨突触起源。缺氧aCSF灌流10-40 min内，VR-MEP的两个成分的振幅均增加至对照组的130-140%，90 min后逐渐下降至对照组的30%，早期成分的潜伏期延长。再氧60分钟后，VR-MEP振幅恢复到80-95%，潜伏期完全恢复，应用抑制性氨基酸拮抗剂士的宁（2 μ M）和印防己毒素（1 μ M）可消除缺氧早期VR-MEP振幅的增加。结果提示，在缺氧早期，由于选择性抑制抑制性突触传递，使VR-MEP波幅增加。

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.