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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Attenuation of abnormal glutamate release in zinc deficiency by zinc and Yokukansan.
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Attenuation of abnormal glutamate release in zinc deficiency by zinc and Yokukansan.

机译：锌和Yokukansan可减轻锌缺乏症患者谷氨酸的异常释放。

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摘要

The mechanism of the abnormal increase in extracellular glutamate concentration in the hippocampus induced with 100mM KCl in zinc deficiency is unknown. In the present study, the changes in glutamate release (exocytosis) and GLT-1, a glial glutamate transporter, expression were studied in young rats fed a zinc-deficient diet for 4 weeks. Exocytosis at mossy fiber boutons was enhanced as reported previously and GLT-1 protein was increased in the hippocampus. The enhanced exocytosis is thought to increase extracellular glutamate concentration. However, the basal concentration of extracellular glutamate in the hippocampus was not increased by zinc deficiency, suggesting that GLT-1 protein increased serves to maintain the basal concentration of extracellular glutamate. The enhanced exocytosis was attenuated in the presence of 100microM ZnCl(2), which attenuated the abnormal increase in extracellular glutamate induced with high K(+) in zinc deficiency. The present study indicates that zinc attenuates abnormal glutamate release in zinc deficiency. The enhanced exocytosis was also attenuated in slices from zinc-deficient rats administered Yokukansan, a herbal medicine, in which the abnormal increase in extracellular glutamate induced with high K(+) was attenuated. It is likely that Yokukansan is useful for prevention or cure of abnormal glutamate release. The enhanced exocytosis in zinc deficiency is a possible mechanism on abnormal increase in extracellular glutamate in the hippocampus induced with high K(+).
机译：缺锌时100mM KCl引起海马细胞外谷氨酸浓度异常增加的机制尚不清楚。在本研究中，在饲喂缺锌饮食4周的年轻大鼠中研究了谷氨酸释放（胞吐作用）和神经胶质谷氨酸转运蛋白GLT-1表达的变化。如先前所报道的，苔藓纤维囊的胞吐作用增强，海马体中的GLT-1蛋白增加。据认为增强的胞吐作用增加了细胞外谷氨酸的浓度。然而，锌缺乏并没有增加海马中细胞外谷氨酸的基础浓度，这表明增加的GLT-1蛋白有助于维持细胞外谷氨酸的基础浓度。增强的胞吐作用在100microM ZnCl（2）的存在下减弱，从而减弱了锌缺乏时高K（+）诱导的细胞外谷氨酸的异常增加。本研究表明锌可减轻锌缺乏症患者谷氨酸的异常释放。服用Yokukansan（一种草药）的缺锌大鼠的切片中，增强的胞吐作用也被减弱，其中高K（+）诱导的细胞外谷氨酸的异常增加被减弱。 Yokukansan很有可能可用于预防或治疗异常的谷氨酸释放。锌缺乏时增强的胞吐作用是高K（+）诱导的海马中细胞外谷氨酸异常增加的可能机制。

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