دورية أكاديمية
أعرض في EDS

Intracerebroventricular administration of okadaic acid induces hippocampal glucose uptake dysfunction and tau phosphorylation.

التفاصيل البيبلوغرافية
العنوان: Intracerebroventricular administration of okadaic acid induces hippocampal glucose uptake dysfunction and tau phosphorylation.
المؤلفون: Broetto N; Neuroscience Post-Graduation Program, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Hansen F; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Brolese G; Neuroscience Post-Graduation Program, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Batassini C; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Lirio F; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Galland F; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Dos Santos JP; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil., Dutra MF; Department of Cellular Biology, Embryology and Genetics, Universidade Federal de Santa Catarina, Florianópolis, Brazil., Gonçalves CA; Neuroscience Post-Graduation Program, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil; Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. Electronic address: casg@ufrgs.br.
المصدر: Brain research bulletin [Brain Res Bull] 2016 Jun; Vol. 124, pp. 136-43. Date of Electronic Publication: 2016 Apr 21.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Country of Publication: United States NLM ID: 7605818 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-2747 (Electronic) Linking ISSN: 03619230 NLM ISO Abbreviation: Brain Res Bull Subsets: MEDLINE
أسماء مطبوعة: Publication: New York Ny : Elsevier Science
Original Publication: Phoenix, N. Y. ANKHO International Inc.
مواضيع طبية MeSH: Enzyme Inhibitors/*administration & dosage , Glucose/*metabolism , Hippocampus/*drug effects , Hippocampus/*metabolism , Okadaic Acid/*administration & dosage, Animals ; Cognition/drug effects ; Dose-Response Relationship, Drug ; Glial Fibrillary Acidic Protein/cerebrospinal fluid ; Glutamate-Ammonia Ligase/metabolism ; Glutamic Acid/metabolism ; Glutathione/metabolism ; In Vitro Techniques ; Injections, Intraventricular ; Male ; Motor Activity/drug effects ; Rats ; Rats, Wistar ; S100 Calcium Binding Protein beta Subunit/cerebrospinal fluid ; S100 Calcium Binding Protein beta Subunit/metabolism ; tau Proteins/metabolism
مستخلص: Intraneuronal aggregates of neurofibrillary tangles (NFTs), together with beta-amyloid plaques and astrogliosis, are histological markers of Alzheimer's disease (AD). The underlying mechanism of sporadic AD remains poorly understood, but abnormal hyperphosphorylation of tau protein is suggested to have a role in NFTs genesis, which leads to neuronal dysfunction and death. Okadaic acid (OKA), a strong inhibitor of protein phosphatase 2A, has been used to induce dementia similar to AD in rats. We herein investigated the effect of intracerebroventricular (ICV) infusion of OKA (100 and 200ng) on hippocampal tau phosphorylation at Ser396, which is considered an important fibrillogenic tau protein site, and on glucose uptake, which is reduced early in AD. ICV infusion of OKA (at 200ng) induced a spatial cognitive deficit, hippocampal astrogliosis (based on GFAP increment) and increase in tau phosphorylation at site 396 in this model. Moreover, we observed a decreased glucose uptake in the hippocampal slices of OKA-treated rats. In vitro exposure of hippocampal slices to OKA altered tau phosphorylation at site 396, without any associated change in glucose uptake activity. Taken together, these findings further our understanding of OKA neurotoxicity, in vivo and vitro, particularly with regard to the role of tau phosphorylation, and reinforce the importance of the OKA dementia model for studying the neurochemical alterations that may occur in AD, such as NFTs and glucose hypometabolism.
(Copyright © 2016 Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: Alzheimer's disease; GFAP; Glucose uptake; Okadaic acid; S100B; Tau phosphorylation
المشرفين على المادة: 0 (Enzyme Inhibitors)
0 (Glial Fibrillary Acidic Protein)
0 (S100 Calcium Binding Protein beta Subunit)
0 (S100b protein, rat)
0 (tau Proteins)
1W21G5Q4N2 (Okadaic Acid)
3KX376GY7L (Glutamic Acid)
EC 6.3.1.2 (Glutamate-Ammonia Ligase)
GAN16C9B8O (Glutathione)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20160426 Date Completed: 20171026 Latest Revision: 20180317
رمز التحديث: 20240628
DOI: 10.1016/j.brainresbull.2016.04.014
PMID: 27108544
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-2747
DOI:10.1016/j.brainresbull.2016.04.014