Department of Neuropsychiatry, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan.
Neurosci Lett. 2012 Nov 30;531(1):10-3. doi: 10.1016/j.neulet.2012.10.013. Epub 2012 Oct 17.
Deficiency of zinc, which modulates glutamate release, might increase ischemic vulnerability of the brain. We examined effects of dietary zinc deficiency for 2 weeks on ischemic vulnerability in several brain regions using dynamic positron autoradiography technique and [18F]2-fluoro-2-deoxy-d-glucose with rat brain slices. In the normal diet group, the cerebral glucose metabolic rate (CMRglc) was not significantly different from that of the ischemia-unloaded control even after the loading of ischemia for 45 min. However, in the zinc-deficient diet group, CMRglc was significantly lower than that of the ischemia-unloaded control after loading of ischemia for 45 min. With treatment of MK-801 (NMDA receptor antagonist) from the start of ischemia loading, CMRglc was not significantly different from that of the ischemia-unloaded control. These findings, obtained for all analyzed brain regions, suggest that dietary zinc deficiency increased ischemic vulnerability in the brain, and that glutamate might contribute to this effect through activation of the NMDA receptor.
锌缺乏会调节谷氨酸的释放，可能会增加大脑的缺血易损性。我们使用动态正电子放射自显影技术和[18F]2-氟-2-脱氧-D-葡萄糖，在大鼠脑切片上研究了 2 周饮食缺锌对几个脑区缺血易损性的影响。在正常饮食组中，即使在缺血负荷 45 分钟后，脑葡萄糖代谢率（CMRglc）与未缺血对照也没有显著差异。然而，在缺锌饮食组中，在缺血负荷 45 分钟后，CMRglc 显著低于未缺血对照。从缺血负荷开始用 MK-801（NMDA 受体拮抗剂）处理后，CMRglc 与未缺血对照没有显著差异。所有分析脑区的这些发现表明，饮食缺锌增加了大脑的缺血易损性，谷氨酸可能通过 NMDA 受体的激活对此产生影响。
