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首页> 外文期刊>Infection and immunity >Neurotoxicity of Clostridium perfringensEpsilon-Toxin for the Rat Hippocampus via the Glutamatergic System
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Neurotoxicity of Clostridium perfringensEpsilon-Toxin for the Rat Hippocampus via the Glutamatergic System

机译：产气荚膜梭菌Epsilon毒素通过谷氨酸能系统对大鼠海马的神经毒性

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摘要

The neurotoxicity of epsilon-toxin, one of the major lethal toxins produced by Clostridium perfringens type B, was studied by histological examination of the rat brain. When the toxin was injected intravenously at a lethal dose (100 ng/kg), neuronal damage was observed in many areas of the brain. Injection of the toxin at a sublethal dose (50 ng/kg) caused neuronal damage predominantly in the hippocampus: pyramidal cells in the hippocampus showed marked shrinkage and karyopyknosis, or so-called dark cells. The dark cells lost the immunoreactivity to microtubule-associated protein-2, a postsynaptic somal and dendric marker, while acetylcholinesterase-positive fibers were not affected. Timm’s zinc staining revealed that zinc ions were depleted in the mossy layers of the CA3 subfield containing glutamate as a synaptic transmitter. The cerebral blood flow in the hippocampus was not altered significantly before or after administration of the toxin, as measured by laser-Doppler flowmetry, excluding the possibility that the observed histological change was due to a secondary effect of ischemia in the hippocampus. Prior injection of either a glutamate release inhibitor or a glutamate receptor antagonist protected the hippocampus from the neuronal damage caused by epsilon-toxin. These results suggest that epsilon-toxin acts on the glutamatergic system and evokes excessive release of glutamate, leading to neuronal damage.
机译：通过对大鼠大脑的组织学检查，研究了产气荚膜梭状芽孢杆菌B型产生的主要致死毒素之一——ε毒素的神经毒性。当以致命剂量（100 ng / kg）静脉注射毒素时，在大脑的许多区域都观察到了神经元损伤。亚致死剂量（50 ng / kg）的毒素注射主要在海马中引起神经元损害：海马中的锥体细胞显示出明显的皱缩和核分裂症，即所谓的暗细胞。深色细胞丧失了对微管相关蛋白2（突触后体细胞和树突状标志物）的免疫反应性，而乙酰胆碱酯酶阳性纤维未受影响。 Timm的锌染色表明，在含有谷氨酸作为突触递质的CA3子域的生苔层中，锌离子被消耗掉了。如通过激光多普勒血流仪测量的那样，在施用毒素之前或之后，海马中的脑血流量没有明显改变，但排除了观察到的组织学改变是由于海马中缺血的继发作用引起的。事先注射谷氨酸释放抑制剂或谷氨酸受体拮抗剂可以保护海马免受ε毒素引起的神经元损害。这些结果表明，ε-毒素作用于谷氨酸能系统并引起谷氨酸的过度释放，从而导致神经元损伤。

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