کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6276932 | 1295746 | 2010 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Persistent gene expression changes in ventral tegmental area of adolescent but not adult rats in response to chronic nicotine
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کلمات کلیدی
IPAN-methyl d-aspartic acidAdolescent drug abuseGCOSVTANMDACPPFDRRT-PCRAcb - ACBSprague–Dawley - اسپراگ داولیnicotine addiction - اعتیاد به نیکوتینIngenuity Pathway Analysis - تجزیه و تحلیل راه Ingenuityconditioned place preference - ترجیح محل موظف استlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Nervous system development - توسعه سیستم عصبیDopamine - دوپامینpost-natal day - روز بعد از تولدfalse discovery rate - میزان کشف کاذبventral tegmental area - ناحیه تگمنتوم شکمیNucleus accumbens - هسته accumbensreverse transcriptase polymerase chain reaction - واکنش زنجیره ای پلی مراز ترانس کریتاز معکوسNicotinic receptors - گیرنده های نیکوتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Because adolescent brains are undergoing extensive developmental changes, they may be uniquely sensitive to effects of addictive drugs like nicotine. We exposed adolescent and adult rats to nicotine infusion for two weeks, and then used whole genome microarray analysis to determine effects on gene expression in the ventral tegmental area. We examined brains immediately after two weeks of nicotine or saline, and also four weeks after termination of nicotine exposure. After identifying genes with a significant ageÃtreatment interaction, we employed template matching to find specific patterns of expression across age and treatment. Of those genes that were transiently regulated (up- or down-regulated immediately following the end of nicotine treatment, but back to saline baseline 30 days later), two-thirds were specific to adult animals, while only 30% were specific to adolescents and 4% were shared across the two ages. In contrast, significant genes that were persistently regulated (altered following nicotine treatment and still altered 30 days later) were more likely (59%) to be adolescent, with only 32% in adults and 8% shared. The greatest number of significant genes was late-regulated (no change immediately after nicotine, but regulated 30 days later). Again, most were in adolescents (54%), compared to adults (10%) or shared (36%). Pathway analysis revealed that adolescent-specific genes were over-represented in several biological functions and canonical pathways, including nervous system development and function and long-term potentiation. Furthermore, adolescent-specific genes formed extensive interaction networks, unlike those specific for adults or shared. This age-specific expression pattern may relate to the heightened vulnerability of adolescents to the effects of addictive drugs. In particular, the propensity of adolescents to show persistent alterations in gene expression corresponds to the persistence of drug dependence among smokers who began their habit as adolescents. These findings support a model whereby adolescent brains are uniquely vulnerable to long-term changes in gene expression in the brain's reward pathway caused by early exposure to nicotine.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 170, Issue 2, 13 October 2010, Pages 503-513
Journal: Neuroscience - Volume 170, Issue 2, 13 October 2010, Pages 503-513
نویسندگان
M.B. Doura, T.V. Luu, N.H. Lee, D.C. Perry,