NMDA 受体的激活拮抗 NMDA 拮抗剂在小鼠高架十字迷宫试验中引起的抗焦虑作用。
NMDA receptor activation antagonizes the NMDA antagonist-induced antianxiety effect in the elevated plus-maze test in mice.
机构信息
Department of Applied Pharmacy, Medical University of Lublin, Chodźki 1, PL 20-093 Lublin, Poland.
出版信息
Pharmacol Rep. 2013;65(5):1124-31. doi: 10.1016/s1734-1140(13)71470-1.
BACKGROUND
The purpose of this study was to determine how the activation of different regulatory domains of the NMDA complex affects the antianxiety effect of antagonists acting at its distinct binding sites.
METHODS
The anxiolytic-like activity was assessed by the elevated plus-maze test in mice.
RESULTS
The anxiolytic activity of CGP 37849 (a competitive NMDA receptor antagonist) and L-701,324 (an antagonist at glycine site) was confirmed, but effects of both were significantly reduced by N-methyl-D-aspartic acid (NMDA) or by D-serine agonists at glutamate and glycine site of the NMDA receptor complex, respectively.
CONCLUSION
The obtained data suggest that stimulation of the glutamate or glycine recognition site of the NMDA receptor complex significantly decreases the antianxiety properties of antagonists of either site.
背景
本研究旨在确定 NMDA 复合物不同调节域的激活如何影响其不同结合位点的拮抗剂的抗焦虑作用。
方法
通过在小鼠中进行高架十字迷宫测试来评估抗焦虑样活性。
结果
CGP 37849（竞争性 NMDA 受体拮抗剂）和 L-701,324（甘氨酸位点拮抗剂）的抗焦虑活性得到了证实，但两者的作用均明显被 N-甲基-D-天冬氨酸（NMDA）或谷氨酸和甘氨酸 NMDA 受体复合物的分别的 D-丝氨酸激动剂所降低。
结论
获得的数据表明，NMDA 受体复合物的谷氨酸或甘氨酸识别位点的刺激显著降低了任一结合位点拮抗剂的抗焦虑特性。
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