کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425764 | 1295890 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of single and continuous administration of amyloid β-peptide (25-35) on adenylyl cyclase activity and the somatostatinergic system in the rat frontal and parietal cortex
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کلمات کلیدی
CREBSRIFIBMXCREAβforskolinPMSF3-isobutyl-1-methylxanthine - 3-ایزوبوتیل-1-متیلکسانتینcyclic AMP - AMP cyclicBSA - BSAcAMP - cAMPamyloid β-peptide - β-پپتید آمیلوئیدadenylyl cyclase - آدنیلات سیکلاز، آدنیلیل سیکلازbovine serum albumin - آلبومین سرم گاوSomatostatin-like immunoreactivity - ایمونواکتیویته مشابه سموتوستاتینAlzheimer’s disease - بیماری آلزایمرSomatostatin - سوماتواستاتینcyclic AMP response element - عنصر پاسخ AMP cyclicphenylmethylsulfonyl fluoride - فنیل متیل سولفونیل فلورایدcerebral cortex - قشر مغزBrain - مغزSomatostatin receptors - گیرنده های سواستوستاتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
It is unknown whether the amyloid β-peptide (Aβ), a principal component found in extracellular neuritic plaques in the brain of patients with Alzheimer's disease (AD), is capable of altering adenylyl cyclase (AC) activity and the somatostatin (SRIF) receptor-effector system in the cerebral cortex of the patients. Therefore, the objective of this study was to investigate the effect of the β fragment, β (25-35), on AC activity and the somatostatinergic system in the rat frontoparietal cortex. A single dose of β (25-35) (10μg) injected intracerebroventricularly significantly decreased the density of SRIF receptors (27.4%) and increased their affinity (32.2%) in the frontoparietal cortex. The inhibitory effect of SRIF on basal and forskolin (FK)-stimulated AC activity was significantly lower in the β (25-35)-treated rats when compared with controls. β (25-35) did not modify Giα1, Giα2 nor Giα3 levels in membranes from the frontoparietal cortex. Continuous infusion of the peptide induced a decrease in the SRIF receptor density in this brain area to a similar extent as that observed 14 days after the single administration of the peptide. Likewise, this treatment decreased the SRIF receptor density in the frontal cortex (15.3%) and parietal cortex (27.2%). This effect was accompanied by a decrease in the SRIF-mediated inhibition of FK-stimulated AC activity (from 41.6% to 25.6%) in the frontal cortex as well by a decrease in basal AC activity (from 36.9% to 31.6%) and FK-stimulated AC activity (from 35.6% to 27.1%) in the parietal cortex. Continuous infusion of Aβ (25-35) had no effect on Giα1, Giα2 or Giα3 levels in membranes from frontal and parietal cortex. However, this treatment caused a decrease in SRIF-like immunoreactivity content in the parietal (38.9%) and frontal (20.4%) cortex. These results suggest that Aβ might be involved in the alterations of somatostatinergic system reported in AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 135, Issue 1, 2005, Pages 181-190
Journal: Neuroscience - Volume 135, Issue 1, 2005, Pages 181-190
نویسندگان
A. Hervás-Aguilar, L. Puebla-Jiménez, E. Burgos-Ramos, D. Aguado-Llera, E. Arilla-Ferreiro,