The entry of manganese ions into the brain is accelerated by the activation of N-methyl-D-aspartate receptors
The entry of manganese ions into the brain is accelerated by the activation of N-methyl-D-aspartate receptors
复制标题
DOI：
10.1016/j.neuroscience.2008.03.080
复制
发表时间：
2008-06-23
期刊：
影响因子：
3.3
通讯作者：
Fujii, H.
中科院分区：
文献类型：
--
作者：
Itoh, K.;Sakata, M.;Fujii, H.
基于锰离子模拟钙离子进入可兴奋细胞的能力，锰增强磁共振成像（MEMRI）作为一种有价值的监测动物大脑生理功能的工具，正受到越来越多的关注。在这里，MEMRI可以在没有预期刺激的情况下检测到锰离子（Mn2+）进入大鼠大脑的可能性进行了测试。这一假设是由于意想不到的观察结果，即与其他麻醉剂（如聚氨酯、戊巴比妥和异氟烷）相比，氯胺酮麻醉大鼠的Mn2+依赖性信号增强被显著抑制。研究了非竞争性n -甲基- d -天冬氨酸受体（NMDAR）拮抗剂氯胺酮和MK-801对MnCl2注射大鼠MEMRI的影响。MK-801治疗比氯胺酮治疗更有效地抑制了信号增强。NMDAR激动剂谷氨酸（100 mg/kg）和n -甲基- d -天冬氨酸（NMDA） （35 mg/kg）增强了MEMRI上的信号强度，这种信号增强被MK-801完全拮抗。NMDAR竞争性拮抗剂d- 2-氨基-5-磷酸戊酸酯（D-AP5）不通过血脑屏障（BBB），对NMDA和谷氨酸诱导的信号增强没有影响。选择性AMPA受体（AMPAR）拮抗剂1,2,3,4-四氢-6-硝基-2,3-二氧基苯并[f]喹啉-7-磺酰胺（NBQX）没有阻断信号增强。这些数据表明，大脑中Mn2+依赖性信号增强是通过NMDAR激活谷氨酸能神经元而不是通过AMPAR激活的结果。(c) 2008 ibro。Elsevier Ltd.出版。版权所有。
Manganese-enhanced magnetic resonance imaging (MEMRI) is receiving increased interest as a valuable tool for monitoring the physiological functions in the animal brain based on the ability of manganese ions to mimic calcium ions entering to excitable cells. Here the possibility that in vivo MEMRI can detect the entry of manganese ions (Mn2+) in the brain of rats behaving without intended stimulation is tested. This hypothesis was a result of the unexpected observation that Mn2+-dependent signal enhancement was dramatically suppressed in ketamine-anesthetized rats compared with other anesthetics, such as urethane, pentobarbital and isoflurane. The effects of noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonists, ketamine and MK-801, on MEMRI for MnCl2 injected rats were examined. Treatment with MK-801 suppressed the signal enhancement more effectively than with ketamine. NMDAR agonists, glutamate (100 mg/kg) and N-methyl-D-aspartate (NMDA) (35 mg/kg), enhanced the signal intensities on MEMRI, and this signal enhancement was completely antagonized by MK-801. The systemic administration of the competitive NMDAR antagonist, D-2-amino-5-phosphono-pentanoate (D-AP5), which does not cross the blood-brain barrier (BBB), showed no effects on the signal enhancement induced by NMDA and glutamate. A selective AMPA receptor (AMPAR) antagonist, 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX), did not block the signal enhancement.These data indicated that the Mn2+-dependent signal enhancement took place as a result of the activation of glutamatergic neurons through NMDAR, but not through AMPAR in the brain. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.