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Glutamate Transporter Inhibitor Advances the Ischemia-induced Depression of Spinal Synaptic Transmission in Rats in vitro

机译:谷氨酸转运蛋白抑制剂在体外大鼠脊柱突触传递的血液突触速度抑制前进

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摘要

Ischemia depresses the spinal la-a motoneuron synaptic transmission via NMDA dependent mechanism. We postulated that glutamate transporter inhibitor (DL-threo-β-hydroxy aspartate, THA) advances the ischemia-induced depression. The experiments were performed on isolated, hemisected spinal cord from 4-6 day old rats. The stimulation of a dorsal root (L_(35)) with supramaximal strength at 0.1 Hz elicited monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Superfusion of ischemic solution (glucose free without O_2 bubbling) depressed the spinal reflexes in a time-dependent manner and abolished them within 50 min. THA alone did not alter the magnitude of MSR and PSR up to 20 min while THA+ischemia abolished the reflexes within 25 min. The abolition time was significantly advanced in THA+ischemia group as compared to ischemia only group. The results indicate that glutamate transporter inhibitor advances the ischemia-induced depression of spinal reflexes substantiating glutamatergic action at this synapse.
机译:缺血通过NMDA依赖机构抑制脊髓LA-A Motoneuron突触传递。我们假设谷氨酸转运蛋白抑制剂(DL-Threo-β-羟基天冬氨酸,THA)推进缺血诱导的抑郁症。从4-6天的老鼠孤立的半殖脊髓进行实验。在相应的节条件根部的0.1Hz引发的单颌骨(MSR)和多腹反射(PSR)电位下,刺激背根(L_(35))的刺激(L_(35))。缺血溶液的叠加(没有O_2鼓泡的葡萄糖)以时间依赖性方式抑制脊柱反射并在50分钟内取消了它们。单独的Tha没有改变MSR和PSR的大小,最多20分钟,而Tha +缺血在25分钟内取消了反应。与缺血群体相比,在+缺血组中,在血液缺血组中取消时间显着提出。结果表明,谷氨酸转运蛋白抑制剂促进血液反射的缺血诱导的抑制在该突触在该突触处的谷氨酸胶作用。

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