摘要
目的:探讨NR2B-pERK-pElk-1途径是否参与了大鼠各学习记忆相关脑区Y-迷宫逃避性学习和记忆。方法:健康雄性成年SD大鼠45只,共分为4组:①ifenprodil腹腔注射组(ifenprodilip,14只),②DMSO腹腔注射组(DMSOip,15只);③ifenprodil脑室注射组(ifenprodilic,8只);④DMSO脑室注射组(DMSO ic,8只)。以Y迷宫训练和测试成绩作为行为学评定指标,用免疫组织化学和Westernblot方法观察大鼠学习记忆相关脑区pERK1/2和pElk-1的变化。结果:Ifenprodilip组与DMSOip组动物的Y迷宫学习成绩没有明显差异(P>0.05),但ifenprodilip组Y迷宫记忆成绩差于DMSOip组(P<0.05)。腹腔注射ifenprodil导致Y迷宫训练后各脑区pERK1/2和pElk-1表达的普遍下降,其中以海马、边缘区、杏仁核最为明显,与DMSOip组相比差异有显著性(P<0.05)。Ifenprodilic组与DMSOic组第一次Y迷宫测试成绩没有明显差异(P>0.05)。第一次测试后立即脑室给药并在给药后6 h测试Y迷宫记忆再巩固成绩,发现ifenprodilic组成绩下降,与DMSOic组相比有明显差异(P<0.05),而且ifenprodilic组动物各脑区的pERK1/2和pElk-1表达与DMSOic组相比均普遍下降,其中pElk-1表达在尾壳核和边缘区几乎完全消失。结论:NR2B对于大鼠Y迷宫长期记忆的形成、记忆再巩固过程是必要的,NR2B的失活将破坏这些过程。同时NR2B的失活减弱了Y迷宫训练后及记忆再巩固测试后学习记忆相关脑区pElk-1和pERK1/2表达,其中在尾壳核和边缘区,NR2B的失活使记忆再巩固测试后pElk-1表达完全被阻断。
Aim： To investigate whether NR2B-pERK1/2-pElk-1 signaling contributes to the Y-maze learning and memory of rat brain. Methods： 45 adult male SD rats were divided into 4 groups： ①Ifenprodil peritoneal injection group（ Ifenprodil ip, n = 14） ; ②DMSO peritoneal injection group（DMSO ip, n = 15） ; ③Ifenprodil cerebral ventricle injection group（ Ifenprodil ic, n = 8） ; ④DMSO cerebral ventricle injection group（DMSO ic, n = 8）. Y-maze training and test were used as an learning and memory enhancing stimulus. Immunohistochemical and Western blotting methods were used for detecting pERK1/2 and pElk-1 expression intensity of different brain regions. Results： Compared with the DMSO ip group, the ifenprodil ip group showed no change on the Y-maze learning score（P〉 0.05）, but its Y-maze memory score tested 24 after learning decreased （P 〈 0.05 ）, Ifenprodil peritoneal injection made brain pERK1/2 and pElk-1 expression decreased generally. In hippocampus, marginal division of striatum（MrD）, amygdala, these changes were more significant（P〈0.05）. Compared with the DMSO ic group, the reconsolidation of Y-maze memory tested 6 hours after ifenprodil injection was impaired in ifenprodil ic group（P〈0.05）. The OD value of pERK1/2 and pElk-1 positive bands in ifenprodil ic group attenuated generally. The pElk- 1 positive bands of caudate putamen and MrD almost disappeared in ifenprodil ic group. Conclusion： NR2B is essential for the formation of long term memory, reconsolidation of Y-maze memory. The deactivation of NR2B by ifenprodil will impair these courses. Meanwhile, the deactivation of NR2B attenuates pERK1/2 and pElk-1 expression of learning and memory related regions after Y-maze learning and memory reconsolidation test. In MrD and candate putamen, the pElk-1 expression are completely blocked by ifenprodil after memory reconsolidation test.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2007年第1期121-125,共5页
Chinese Journal of Applied Physiology
