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锌缺乏时海马体中谷氨酸和γ-氨基丁酸的释放

Release of glutamate and GABA in the hippocampus under zinc deficiency.

作者信息

Takeda Atsushi, Hirate Maki, Tamano Haruna, Oku Naoto

机构信息

Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52- 1 Yada, Shizuoka 422-8526, Japan.

出版信息

J Neurosci Res. 2003 May 15;72(4):537-42. doi: 10.1002/jnr.10600.

Abstract

Zinc homeostasis in the brain is affected by dietary zinc deficiency, and its alteration may cause brain dysfunctions. On the basis of the previous evidence that hippocampal zinc was responsive to 12-week zinc deprivation, responsiveness of hippocampal zinc to dietary zinc deficiency was examined in rats fed a zinc-deficient diet for 4 weeks. Zinc concentration in the hippocampus was not decreased by zinc deprivation for 4 weeks. However, Timm's stain was extensively attenuated in the brain of the zinc-deficient rats. In the brain of the zinc-deficient rats, moreover, zinc concentration in the hippocampal extracellular fluid was approximately 30% of that of control rats. These results demonstrate that vesicular zinc is responsive to dietary zinc and may decrease easily under zinc deficiency. Zinc concentration in the hippocampal extracellular fluid during stimulation with high K(+) was significantly increased even in zinc-deficient rats, although the increased levels of zinc were lower than the basal levels of zinc in control rats. The basal glutamate concentration in the hippocampal extracellular fluid was not significantly different between the control and zinc-deficient rats. However, glutamate concentration in the hippocampal extracellular fluid during stimulation with high K(+) was more increased in the zinc-deficient rats than in the control rats. Gamma aminobutyric acid (GABA) concentration in the hippocampal extracellular fluid during stimulation with high K(+) was increased in the control rats, but not in the zinc-deficient rats. The present study suggests that the excitability of hippocampal glutamatergic neurons is enhanced by dietary zinc deficiency.

摘要

大脑中的锌稳态受饮食中锌缺乏的影响,其改变可能导致脑功能障碍。基于先前海马体锌对12周锌剥夺有反应的证据,在喂食缺锌饮食4周的大鼠中检测了海马体锌对饮食锌缺乏的反应。4周的锌剥夺并未使海马体中的锌浓度降低。然而,缺锌大鼠大脑中的Timm染色明显减弱。此外,在缺锌大鼠的大脑中,海马体细胞外液中的锌浓度约为对照大鼠的30%。这些结果表明,囊泡锌对饮食锌有反应,并且在锌缺乏时可能容易减少。即使在缺锌大鼠中,高钾刺激期间海马体细胞外液中的锌浓度也显著增加,尽管增加的锌水平低于对照大鼠的锌基础水平。对照大鼠和缺锌大鼠海马体细胞外液中的基础谷氨酸浓度没有显著差异。然而,高钾刺激期间,缺锌大鼠海马体细胞外液中的谷氨酸浓度比对照大鼠增加得更多。高钾刺激期间,对照大鼠海马体细胞外液中的γ-氨基丁酸(GABA)浓度增加,而缺锌大鼠则没有。本研究表明,饮食锌缺乏会增强海马体谷氨酸能神经元的兴奋性。

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