Nasehi Mohammad, Hajikhani Marziyeh, Ebrahimi-Ghiri Mohaddeseh, Zarrindast Mohammad-Reza
Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran.
Department of Pharmacology and Toxicology, Islamic Azad University, Pharmaceutical Science Branch (IAUPS), Tehran, Iran.
Psychopharmacology (Berl). 2017 Feb;234(3):507-514. doi: 10.1007/s00213-016-4481-9. Epub 2016 Nov 17.
Convincing evidence has supported the pivotal role of N-methyl-D-aspartate receptors (NMDARs) and CB2Rs in the regulation of learning and memory.
In this study, the role of hippocampal (CA1 region) CB2 receptors on aversive memory consolidation deficit induced by D-AP5, a NMDA receptor antagonist, was evaluated.
Adult male Wistar rats received cannula implants that bilaterally targeted the CA1 region. Long-term memory was examined using the step-through type of passive avoidance task.
Post-training, intra-CA1 microinjection of D-AP5 (0.5 and 0.75 μg/rat), GP1a (CB2 receptor agonist at dose of 150 ng/rat) and AM630 (CB2 receptor antagonist at doses 75 and 100 ng/rat) impaired memory consolidation processes. Intra-CA1 microinjection of a lower dose of GP1a or AM630 restored memory impairment induced by D-AP5 at the two higher doses, while AM630 decreased D-AP5 memory response at the lower dose. The isobologram analysis showed that there is a synergistic effect between D-AP5 and AM630 on memory consolidation deficit.
These results suggest that CA1 CB2 receptors modulate memory consolidation impairment induced by D-AP5.
确凿的证据支持了N-甲基-D-天冬氨酸受体（NMDARs）和CB2Rs在学习和记忆调节中的关键作用。
在本研究中，评估了海马体（CA1区）CB2受体在NMDA受体拮抗剂D-AP5诱导的厌恶记忆巩固缺陷中的作用。
成年雄性Wistar大鼠接受双侧靶向CA1区的套管植入。使用穿梭箱式被动回避任务检查长期记忆。
训练后，向CA1区内微量注射D-AP5（0.5和0.75μg/只大鼠）、GP1a（CB2受体激动剂，剂量为150ng/只大鼠）和AM630（CB2受体拮抗剂，剂量为75和100ng/只大鼠）会损害记忆巩固过程。向CA1区内微量注射较低剂量的GP1a或AM630可恢复由较高剂量的D-AP5诱导的记忆损伤，而AM630在较低剂量时可降低D-AP5的记忆反应。等效线图分析表明，D-AP5和AM630在记忆巩固缺陷方面存在协同作用。
这些结果表明，CA1区CB2受体可调节由D-AP5诱导的记忆巩固损伤。
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