کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478549 | 1551138 | 2015 | 40 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nicotine recruits glutamate receptors to postsynaptic sites
ترجمه فارسی عنوان
نیکوتین گیرنده های گلوتامات را به سایت های پست پاتولوژیک جذب می کند
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
PBSGluN2B-containing NMDA receptorNASPMGluAE/ImEPSCsnAChRsEPSCsIPSCsAPVN-methyl-d-aspartateNMDAMLAAMPAGAPDH6-Cyano-7-nitroquinoxaline-2,3-dione - 6-Cyano-7-nitroquinoxaline-2،3-dioneBSA - BSADHβE - DHBAEbovine serum albumin - آلبومین سرم گاوDL-2-Amino-5-phosphonopentanoic acid - اسید DL-2-آمینو-5-فسفونوپنتانوئیکα-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid - اسید α-آمینو 3-هیدروکسی-5-متیل-4-ایزوکسول پپونیکANOVA - تحلیل واریانس Analysis of varianceone-way analysis of variance - تحلیل واریانس یک راههlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP excitatory postsynaptic currents - جریان های پسینپتیک هیجان انگیزinhibitory postsynaptic currents - جریانهای پسینپتیک مهارکنندهdihydro-β-erythroidine - دی هیدرو-β-erythroidineCNQX - سیانکیوایکسSynapses - سیناپس هاmethyllycaconitine - متیل لیکاکونیتینPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریNicotine - نیکوتین Nicotinic - نیکوتینیکHippocampus - هیپوکامپ glutamatergic - گلوتاماترگیکglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازNMDA receptors - گیرنده NMDAAMPA receptors - گیرنده های AMPAnicotinic acetylcholine receptors - گیرنده های استیل کولین نیکوتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
Cholinergic neurons project throughout the nervous system and activate nicotinic receptors to modulate synaptic function in ways that shape higher order brain function. The acute effects of nicotinic signaling on long-term synaptic plasticity have been well-characterized. Less well understood is how chronic exposure to low levels of nicotine, such as those encountered by habitual smokers, can alter neural connections to promote addiction and other lasting behavioral effects. We show here that chronic exposure of hippocampal neurons in culture to low levels of nicotine recruits AMPA and NMDA receptors to the cell surface and sequesters them at postsynaptic sites. The receptors include GluA2-containing AMPA receptors, which are responsible for most of the excitatory postsynaptic current mediated by AMPA receptors on the neurons, and include NMDA receptors containing GluN1 and GluN2B subunits. Moreover, we find that the nicotine treatment also increases expression of the presynaptic component synapsin 1 and arranges it in puncta juxtaposed to the additional AMPA and NMDA receptor puncta, suggestive of increases in synaptic contacts. Consistent with increased synaptic input, we find that the nicotine treatment leads to an increase in the excitatory postsynaptic currents mediated by AMPA and NMDA receptors. Further, the increases skew the ratio of excitatory-to-inhibitory input that the cell receives, and this holds both for pyramidal neurons and inhibitory neurons in the hippocampal CA1 region. The GluN2B-containing NMDA receptor redistribution at synapses is associated with a significant increase in GluN2B phosphorylation at Tyr1472, a site known to prevent GluN2B endocytosis. These results suggest that chronic exposure to low levels of nicotine not only alters functional connections but also is likely to change excitability levels across networks. Further, it may increase the propensity for synaptic plasticity, given the increase in synaptic NMDA receptors.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 68, September 2015, Pages 340-349
Journal: Molecular and Cellular Neuroscience - Volume 68, September 2015, Pages 340-349
نویسندگان
Jing-jing Duan, Adrian F. Lozada, Chen-yu Gou, Jing Xu, Yuan Chen, Darwin K. Berg,