کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271814 | 1614773 | 2015 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chronic maternal hyperglycemia induced during mid-pregnancy in rats increases RAGE expression, augments hippocampal excitability, and alters behavior of the offspring
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کلمات کلیدی
KCNKHEPESPNDEGTAPPITTCGDMAGEsRAGEFR1HMGB1STZ4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazineethanesulfonic acidethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدNeurodevelopmental disorder - اختلال نوروپاتولوژیstreptozotocin - استرپتوزوتوسینBehavioral flexibility - انعطاف پذیری رفتاریanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancelong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Recognition memory - حافظه تشخیص یا شناختGestational diabetes mellitus - دیابت بارداریGestational diabetes - دیابت بارداریgestational day - روز بارداریpostnatal day - روز پس از زایمانadvanced glycation end-products - محصولات نهایی گلیسایی پیشرفتهPrepulse inhibition - مهار پیش قاعدگیfixed ratio 1 - نسبت ثابت 1Hippocampus - هیپوکامپ High-mobility group Box-1 - گروه حمل و نقل بالا Box-1Sensorimotor gating - گیت سنترReceptor for advanced glycation end-products - گیرنده برای پایان دادن به محصولات glycation پیشرفته
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Maternal diabetes during pregnancy may increase the risk of neurodevelopmental disorders in the offspring by increasing inflammation. A major source of inflammatory signaling observed in diabetes is activation of the receptor for advanced glycation end-products (RAGE), and increased RAGE expression has been reported in psychiatric disorders. Thus, we sought to examine whether maternal diabetes creates a proinflammatory state, triggered largely by RAGE signaling, that alters normal brain development and behavior of the offspring. We tested this hypothesis in rats using the streptozotocin (STZ; 50Â mg/kg; i.p.) model of diabetes induced during mid-pregnancy. Following STZ treatment, we observed a significant increase in RAGE protein expression in the forebrain of the offspring (postnatal day 1). Data obtained from whole-cell patch clamping of hippocampal neurons in cultures from the offspring of STZ-treated dams revealed a striking increase in excitability. When tested in a battery of behavioral tasks in early adulthood, the offspring of STZ-treated dams had significantly lower prepulse inhibition, reduced anxiety-like behavior, and altered object-place preference when compared to control offspring. In an operant-based strategy set-shifting task, STZ offspring did not differ from controls on an initial visual discrimination or reversal learning but took significantly longer to shift to a new strategy (i.e., set-shift). Insulin replacement with an implantable pellet in the dams reversed the effects of maternal diabetes on RAGE expression, hippocampal excitability, prepulse inhibition and object-place memory, but not anxiety-like behavior or set-shifting. Taken together, these results suggest that chronic maternal hyperglycemia alters normal hippocampal development and behavior of the offspring, effects that may be mediated by increased RAGE signaling in the fetal brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 303, 10 September 2015, Pages 241-260
Journal: Neuroscience - Volume 303, 10 September 2015, Pages 241-260
نویسندگان
A.R. Chandna, N. Kuhlmann, C.A. Bryce, Q. Greba, V.A. Campanucci, J.G. Howland,