کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8840674 | 1614693 | 2018 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure
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کلمات کلیدی
PBSFASDsEtOHSSTBECsDAPIGCLEthanol - اتانولFetal alcohol spectrum disorders - اختلالات طیف الکل جنینgamma-aminobutyric acid - اسید گاما آمینو بوتیریکAlcohol - الکلInterneuron - اینترنورون، نورون رابط، نورون بینابینیfetal - جنینApoptosis - خزان یاختهایDevelopment - رشدSomatostatin - سوماتواستاتینgranule cell layer - لایه سلول گرانولPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریHippocampus - هیپوکامپ Parvalbumin - پاروالبومینGABA - گابا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure](/preview/png/8840674.png)
چکیده انگلیسی
Developmental exposure to ethanol leads to a constellation of cognitive and behavioral abnormalities known as Fetal Alcohol Spectrum Disorders (FASDs). Many cell types throughout the central nervous system are negatively impacted by gestational alcohol exposure, including inhibitory, GABAergic interneurons. Little evidence exists, however, describing the long-term impact of fetal alcohol exposure on survival of interneurons within the hippocampal formation, which is critical for learning and memory processes that are impaired in individuals with FASDs. Mice expressing Venus yellow fluorescent protein in inhibitory interneurons were exposed to vaporized ethanol during the third trimester equivalent of human gestation (postnatal days 2-9), and the long-term effects on interneuron numbers were measured using unbiased stereology at P90. In adulthood, interneuron populations were reduced in every hippocampal region examined. Moreover, we found that a single exposure to ethanol at P7 caused robust activation of apoptotic neurodegeneration of interneurons in the hilus, granule cell layer, CA1 and CA3 regions of the hippocampus. These studies demonstrate that developmental ethanol exposure has a long-term impact on hippocampal interneuron survivability, and may provide a mechanism partially explaining deficits in hippocampal function and hippocampus-dependent behaviors in those afflicted with FASDs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 383, 15 July 2018, Pages 60-73
Journal: Neuroscience - Volume 383, 15 July 2018, Pages 60-73
نویسندگان
Clark W. Bird, Devin H. Taylor, Natalie J. Pinkowski, G. Jill Chavez, C. Fernando Valenzuela,