نقش گیرندههای متابوتروپیکی تیپ گلوتامات(mGLu4)هسته اکومبنس در شرطی شدن مکانی القاء شده توسط مرفین در موشهای بزرگ آزمایشگاهی نر.

Autor: زهرا ابراهیمی, نازنین کهوندی, الهه شهریاری, علیرضا کمکی, سید اسعد کریمی, مریم شریفی, عبدالرحمن صریحی
Předmět:
Zdroj: Koomesh: Journal of Semnan University of Medical Sciences; Sep/Oct2023, Vol. 25 Issue 5, p237-237, 2p
Abstrakt: Introduction: Metabotropic glutamate receptors (mGluRs) in the nucleus accumbens (NAc) play an important role in the reward pathway. In addition, several studies have shown that glutamate neurotransmission in the NAc is required for the development of morphine-induced conditioned place preference (CPP). Methods and Materials: In the present study, the effect of bilateral intraluminal injection of VU0155041 (VU), a positive allosteric modulator and partial agonist of mGluR4 on the acquisition, expression, extinction, and reinstatement of CPP induced by morphine in male rats was investigated. In Experiment 1, the VU was administered at doses of 10, 30, and 50 μg/0.5 μL saline per side into the NAc during the 3 days of morphine (5 mg/kg) conditioning (acquisition) phase of morphine-induced CPP. In Experiment 2, rats received VU at the dose of 50 μg/0.5 μL, 5 min before the post-conditioning test in order to check the effect of VU0155041 on the expression of morphine-induced CPP. In Experiment 3, VU (10, 30, and 50 μg/0.5 μL) was injected during the extinction period, and In Experiment 4, the CPP extinguished rats received VU (10, 30, and 50 μg/0.5 μL) five minutes prior to the administration of morphine (1 mg/kg) in order to reinstate the extinguished CPP. Results: The results showed that the intra-accumbal injection of VU inhibits the acquisition of morphine-induced CPP in a dose-dependent manner, but has no effect on expression and reduced the extinction period of CPP. Furthermore, the administration of VU into the NAc dose-dependently inhibited the reinstatement of morphine-CPP. Conclusion: These effects may be related to changes in glutamate activity in the NAC and/or the learning dependent mechanism of glutamate neurotransmission in the reward pathway. [ABSTRACT FROM AUTHOR]
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