کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6016844 | 1580152 | 2016 | 26 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Consequences of excessive plasticity in the hippocampus induced by perinatal asphyxia
ترجمه فارسی عنوان
پیامدهای پلاستیکی بیش از حد در هیپوکامپ ناشی از آسفیکسی پریناتال
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کلمات کلیدی
PI3KGFAPSynaptogenesisNeuNGSK3MAP-2NDDSm6A - m6aPhosphatidylinositol-4,5-bisphosphate 3-kinase - Phosphatidylinositol-4،5-bisphosphate 3-kinaseβ-actin - β-اکتینOpen field test - آزمایش میدان بازPerinatal asphyxia - آسفیکسی پریناتالNeurodevelopmental disorders - اختلالات عصبی توسعهGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالneuron-specific nuclear protein - پروتئین هسته ای اختصاصی نورونglycogen synthase kinase 3 - گلیکوزین سنتاز کیناز 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
چکیده انگلیسی
Perinatal asphyxia (PA) is one of the most frequent risk factors for several neurodevelopmental disorders (NDDs) of presumed multifactorial etiology. Dysfunction of neuronal connectivity is thought to play a central role in the pathophysiology of NDDs. Because underlying causes of some NDDs begin before/during birth, we asked whether this clinical condition might affect accurate establishment of neural circuits in the hippocampus as a consequence of disturbed brain plasticity. We used a murine model that mimics the pathophysiological processes of perinatal asphyxia. Histological analyses of neurons (NeuN), dendrites (MAP-2), neurofilaments (NF-M/Hp) and correlative electron microscopy studies of dendritic spines were performed in Stratum radiatum of the hippocampal CA1 area after postnatal ontogenesis. Protein and mRNA analyses were achieved by Western blot and RT-qPCR. Behavioral tests were also carried out. NeuN abnormal staining and spine density were increased. RT-qPCR assays revealed a β-actin mRNA over-expression, while Western blot analysis showed higher β-actin protein levels in synaptosomal fractions in experimental group. M6a expression, protein involved in filopodium formation and synaptogenesis, was also increased. Furthermore, we found that PI3K/Akt/GSK3 pathway signaling, which is involved in synaptogenesis, was activated. Moreover, asphyctic animals showed habituation memory changes in the open field test. Our results suggest that abnormal synaptogenesis induced by PA as a consequence of excessive brain plasticity during brain development may contribute to the etiology of the NDDs. Consequences of this altered synaptic maturation can underlie some of the later behavioral deficits observed in NDDs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 286, December 2016, Pages 116-123
Journal: Experimental Neurology - Volume 286, December 2016, Pages 116-123
نویسندگان
G.E. Saraceno, L.G. Caceres, L.R. Guelman, R. Castilla, L.D. Udovin, M.H. Ellisman, M.A. Brocco, F. Capani,