کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6255983 | 1612922 | 2016 | 9 صفحه PDF | دانلود رایگان |
- Over-expression of GluN2B subunits facilitated the acquisition of morphine CPP.
- GluN2B transgenic rats showed more vulnerability to naloxone-induced CPA.
- Over-expression of GluN2B subunits had no effect on natural reward-induced CPP.
GluN2B-containing N-methyl-d-aspartate (NMDA) receptors in the brain are known to have an important role in drug-associated learning and memory. Selective blockage of GluN2B-containing NMDA receptors (GluN2B-NMDARs) has been shown to impair morphine-induced conditioned place preference (CPP) without affecting natural reward-induced CPP. In the present study, GluN2B transgenic rats with over-expressed GluN2B-subunits in the forebrain were used to assess the susceptibility to CPP induced by morphine and natural rewards as well as to naloxone-induced conditioned place aversion (CPA). The results showed that GluN2B transgenic rats exhibited a relatively higher susceptibility to morphine-induced CPP and naloxone-induced CPA than their wild-type littermates did, while they retained the similar sensitivity as wild-type rats to CPP induced by natural reinforcers (food and sucrose). These findings suggest that increased level of GluN2B-NMDARs in forebrain facilitates formation of drug-related memory, but not that associated with natural rewards. GluN2B-NMDARs might be a potential target for the treatment of drug abuse.
Journal: Behavioural Brain Research - Volume 311, 15 September 2016, Pages 416-424