Abstract：
The current study was designed to examine the role of glutamate NMDA receptors of the mediodorsal thalamus (MD) in scopolamine-induced memory impairment. Adult male rats were bilaterally cannulated into the MD. According to the results, intraperitoneal (i.p.) administration of scopolamine (1.5 mg/kg) immediately after the training phase (post-training) impaired memory consolidation. Bilateral microinjection of the glutamate NMDA receptors agonist, N-Methyl-D-aspartic acid (NMDA; 0.05 µg/rat), into the MD significantly improved scopolamine-induced memory consolidation impairment. Co-administration of D-AP5, a glutamate NMDA receptor antagonist (0.001-0.005 µg/rat, intra-MD) potentiated the response of an ineffective dose of scopolamine (0.5 mg/kg, i.p.) to impair memory consolidation, mimicking the response of a higher dose of scopolamine. Noteworthy, post-training intra-MD microinjections of the same doses of NMDA or D-AP5 alone had no effect on memory consolidation. Moreover, the blockade of the glutamate NMDA receptors by 0.003 ng/rat of D-AP5 prevented the improving effect of NMDA on scopolamine-induced amnesia. Thus, it can be concluded that the MD glutamatergic system may be involved in scopolamine-induced memory impairment via the NMDA receptor signaling pathway.
摘要：
本研究旨在研究中丘脑（MD）的谷氨酸NMDA受体在东pol碱诱导的记忆障碍中的作用。将成年雄性大鼠双侧插管入MD。根据结果,训练阶段（训练后）后立即腹膜内（i.p.）给予东pol碱（1.5mg/kg），记忆巩固受损。双侧显微注射谷氨酸NMDA受体激动剂，N-甲基-D-天冬氨酸（NMDA;0.05µg/大鼠），进入MD显着改善东pol碱诱导的记忆巩固障碍。D-AP5，一种谷氨酸NMDA受体拮抗剂（0.001-0.005µg/大鼠，MD内）增强了无效剂量的东莨菪碱（0.5mg/kg，i.p.)损害记忆巩固，模仿较高剂量的东pol碱的反应。值得注意的是,训练后MD内显微注射相同剂量的NMDA或D-AP5对记忆巩固没有影响.此外，0.003ng/大鼠D-AP5对谷氨酸NMDA受体的阻断阻止了NMDA对东莨菪碱引起的健忘症的改善作用。因此，可以得出结论，MD谷氨酸能系统可能通过NMDA受体信号通路参与东莨菪碱诱导的记忆障碍。
