Czéh G, Somjen G G
Division of Physiology, Duke University Medical Center, Durham, NC 27710.
Brain Res. 1990 Sep 17;527(2):224-33. doi: 10.1016/0006-8993(90)91141-3.
Responses evoked by stimulation of a dorsal root were recorded from ventral and dorsal roots of isolated spinal cords of infant mice. Interstitial potassium, [K+]o, and extracellular DC voltage were recorded from dorsal gray matter in some experiments. When oxygen was withdrawn, synaptically transmitted discharges (dorsal horn response, DHR, and monosynaptic ventral root reflex, VRR) began to be depressed within a minute, and were depressed to less than 30% of control amplitude in 10-15 min. Responses recovered fully if oxygen was readmitted within 45 min, but no recovery was seen after 90 min of hypoxia. The degree of the depression of VRR was as expected from the depression of the electrotonically conducted excitatory postsynaptic potential (VRepsp). Responses failed much more rapidly in spinal cords of 15-16-day-old mice, than of 9-14-day-olds. When the spinal cord was bathed in elevated [Ca2+]o or in reduced [Mg2+]o, synaptic transmission was consistently maintained for a longer period of hypoxia than in bathing fluid of normal cation content. In a sizeable minority of the trials during hypoxia an abrupt increase of [K+]o occurred, accompanied by a sudden negative shift of extracellular potential, closely resembling spreading depression (SD) of forebrain structures. Delayed post-hypoxic spontaneous activity was seen in many spinal cords. The results are compatible with the hypothesis that hypoxic failure of synaptic transmission is due, in part or whole, to blockade of inward Ca2(+)-current in presynaptic terminals. Cells in spinal gray matter can no longer be regarded as 'immune' to SD-like depolarization, but the limited conditions under which SD can occur are not yet clear.
从新生小鼠分离脊髓的腹根和背根记录刺激背根所诱发的反应。在一些实验中，从背侧灰质记录间质钾离子浓度（[K⁺]o）和细胞外直流电压。当停止供氧时，突触传递的放电（背角反应，DHR，和单突触腹根反射，VRR）在一分钟内开始受到抑制，并在10 - 15分钟内被抑制到对照幅度的30%以下。如果在45分钟内重新供氧，反应可完全恢复，但缺氧90分钟后则未见恢复。VRR的抑制程度与电紧张性传导的兴奋性突触后电位（VRepsp）的抑制情况相符。15 - 16日龄小鼠脊髓中的反应比9 - 14日龄小鼠的更快消失。当脊髓浸浴在高[Ca²⁺]o或低[Mg²⁺]o的溶液中时，与正常阳离子含量的浴液相比，突触传递在缺氧时能持续更长时间。在缺氧期间的相当一部分试验中，[K⁺]o突然升高，同时细胞外电位突然负向偏移，这与前脑结构的扩散性抑制（SD）极为相似。许多脊髓中出现了缺氧后延迟的自发活动。这些结果与以下假设相符，即突触传递的缺氧性衰竭部分或全部归因于突触前终末内向Ca²⁺电流的阻断。脊髓灰质中的细胞不能再被视为对类似SD的去极化“免疫”，但SD能够发生的有限条件尚不清楚。
