کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2564844 1561043 2014 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Dopamine decreases NMDA currents in the oval bed nucleus of the stria terminalis of cocaine self-administering rats
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی روانپزشکی بیولوژیکی
پیش نمایش صفحه اول مقاله
Dopamine decreases NMDA currents in the oval bed nucleus of the stria terminalis of cocaine self-administering rats
چکیده انگلیسی


• Dopamine reduced NMDA currents in the ovBNST of cocaine self-administering rats.
• Dopamine reduced NMDA currents through G-protein/PLC/phosphatase D1R and D2R.
• Dopamine preferentially reduced GluN2A-containing NMDA currents.

Dopamine (DA) and N-methyl-d-aspartate receptors (NMDARs) contribute in the neural processes underlying drug-driven behaviors. DA is a potent modulator of NMDAR, but few studies have investigated the functional interaction between DA and NMDAR in the context of substance abuse. We combined the rat model of cocaine self-administration with brain slice electrophysiology to study DA modulation of NMDA currents in the oval bed nucleus of the stria terminalis (ovBNST), a dense DA terminal field involved in maintenance of cocaine self-administration amongst other drug related behaviors. Long-Evans rats self-administered intravenous cocaine (0.75 mg/kg/injection) on a progressive ratio (PR) schedule of reinforcement for 15 days and whole-cell patch-clamp recordings were done on the 16th day. DA reduced NMDA currents in brain-slices from cocaine self-administering rats, but not in those of drug-naïve and sucrose self-administering, or when cocaine exposure was passive (yoked), revealing a mechanism unique to voluntary cocaine intake. DA reduced NMDA currents by activating G-protein-coupled D1- and D2-like receptors that converged on phospholipase C and protein phosphatases. Accordingly, our study reveals a mechanism that may contribute to dysfunctional synaptic plasticity associated with drug-driven behaviors during acute withdrawal.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 51, 3 June 2014, Pages 83–88
نویسندگان
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