دورية أكاديمية
أعرض في EDS

G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channel Activation by the p75 Neurotrophin Receptor Is Required for Amyloid β Toxicity.

التفاصيل البيبلوغرافية
العنوان: G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channel Activation by the p75 Neurotrophin Receptor Is Required for Amyloid β Toxicity.
المؤلفون: May LM; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia., Anggono V; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia.; Clem Jones Centre for Ageing Dementia Research, University of QueenslandBrisbane, QLD, Australia., Gooch HM; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia., Jang SE; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia.; Clem Jones Centre for Ageing Dementia Research, University of QueenslandBrisbane, QLD, Australia., Matusica D; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia.; Centre for Neuroscience, College of Medicine and Public Health, Flinders UniversityAdelaide, SA, Australia., Kerbler GM; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia., Meunier FA; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia.; Clem Jones Centre for Ageing Dementia Research, University of QueenslandBrisbane, QLD, Australia., Sah P; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia., Coulson EJ; Queensland Brain Institute, University of QueenslandBrisbane, QLD, Australia.; Clem Jones Centre for Ageing Dementia Research, University of QueenslandBrisbane, QLD, Australia.; School of Biomedical Sciences, University of QueenslandBrisbane, QLD, Australia.
المصدر: Frontiers in neuroscience [Front Neurosci] 2017 Aug 08; Vol. 11, pp. 455. Date of Electronic Publication: 2017 Aug 08 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101478481 Publication Model: eCollection Cited Medium: Print ISSN: 1662-4548 (Print) Linking ISSN: 1662453X NLM ISO Abbreviation: Front Neurosci Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Research Foundation
مستخلص: Alzheimer's disease is characterized by cognitive decline, neuronal degeneration, and the accumulation of amyloid-beta (Aβ). Although, the neurotoxic Aβ peptide is widely believed to trigger neuronal dysfunction and degeneration in Alzheimer's disease, the mechanism by which this occurs is poorly defined. Here we describe a novel, Aβ-triggered apoptotic pathway in which Aβ treatment leads to the upregulation of G-protein activated inwardly rectifying potassium (GIRK/Kir3) channels, causing potassium efflux from neurons and Aβ-mediated apoptosis. Although, GIRK channel activity is required for Aβ-induced neuronal degeneration, we show that it is not sufficient, with coincident signaling by the p75 neurotrophin receptor (p75 NTR ) also required for potassium efflux and cell death. Our results identify a novel role for GIRK channels in mediating apoptosis, and provide a previously missing mechanistic link between the excitotoxicity of Aβ and its ability to trigger cell death pathways, such as that mediated by p75 NTR . We propose that this death-signaling pathway contributes to the dysfunction of neurons in Alzheimer's disease and is responsible for their eventual degeneration.
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فهرسة مساهمة: Keywords: Alzheimer's disease; GIRK channel; Kir3; amyloid β; excitotoxicity; neurodegeneration; p75NTR; potassium flux
تواريخ الأحداث: Date Created: 20170830 Latest Revision: 20200929
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC5550722
DOI: 10.3389/fnins.2017.00455
PMID: 28848381
قاعدة البيانات: MEDLINE
الوصف
تدمد:1662-4548
DOI:10.3389/fnins.2017.00455