کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5814656 | 1556635 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Prolonged nicotine exposure down-regulates presynaptic NMDA receptors in dopaminergic terminals of the rat nucleus accumbens
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کلمات کلیدی
PBSCalcium levelsT-TBSNACN-methyl-d-aspartic acidDATAMPAnAChRsECLNMDABSA - BSADHβE - DHBAEFura-2AM - FURA-02:00bovine serum albumin - آلبومین سرم گاوACh - آهAcetylcholine - استیل کولینneurotransmitter release - انتشار نوروترانسمیترDopamine transporter - انتقال دهنده دوپامینenhanced chemiluminescence - بهبود شیمیایی لومنDopamine - دوپامینdihydro-β-erythroidine - دی هیدرو-β-erythroidineSynaptosomes - سیناپتوزوم هاSyn - سینتFura-2-acetoxymethyl ester - فورا 2-اتوکسی متیل استرpre - قبل ازPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریNucleus accumbens - هسته accumbenspost - پستNMDA receptors - گیرنده NMDAnicotinic acetylcholine receptors - گیرنده های استیل کولین نیکوتینNicotinic receptors - گیرنده های نیکوتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
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چکیده انگلیسی
The presynaptic control of dopamine release in the nucleus accumbens (NAc) by glutamate and acetylcholine has a profound impact on reward signaling. Here we provide immunocytochemical and neurochemical evidence supporting the co-localization and functional interaction between nicotinic acetylcholine receptors (nAChRs) and N-methyl-D-aspartic acid (NMDA) receptors in dopaminergic terminals of the NAc. Most NAc dopaminergic terminals possessed the nAChR α4 subunit and the pre-exposure of synaptosomes to nicotine (30 μM) or to the α4β2-containing nAChR agonist 5IA85380 (10 nM) selectively inhibited the NMDA (100 μM)-evoked, but not the 4-aminopyridine (10 μM)-evoked, [3H] dopamine outflow; this inhibition was blunted by mecamylamine (10 μM). Nicotine and 5IA85380 pretreatment also inhibited the NMDA (100 μM)-evoked increase of calcium levels in single nerve terminals, an effect prevented by dihydro-β-erythroidine (1 μM). This supports a functional interaction between α4β2-containing nAChR and NMDA receptors within the same terminal, as supported by the immunocytochemical co-localization of α4 and GluN1 subunits in individual NAc dopaminergic terminals. The NMDA-evoked [3H]dopamine outflow was blocked by MK801 (1 μM) and inhibited by the selective GluN2B-selective antagonists ifenprodil (1 μM) and RO 25-6981 (1 μM), but not by the GluN2A-preferring antagonists CPP-19755 (1 μM) and ZnCl2 (1 nM). Notably, nicotine pretreatment significantly decreased the density of biotin-tagged GluN2B proteins in NAc synaptosomes. These results show that nAChRs dynamically and negatively regulate NMDA receptors in NAc dopaminergic terminals through the internalization of GluN2B receptors.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 79, April 2014, Pages 488-497
Journal: Neuropharmacology - Volume 79, April 2014, Pages 488-497
نویسندگان
Alessia Salamone, Stefania Zappettini, Massimo Grilli, Guendalina Olivero, Paula Agostinho, Angelo R. Tomé, Jiayang Chen, Anna Pittaluga, Rodrigo A. Cunha, Mario Marchi,