Amyloid-β(25-35) Modulates the Expression of GirK and KCNQ Channel Genes in the Hippocampus

During early stages of Alzheimer's disease (AD), synaptic dysfunction induced by toxic amyloid-β (Aβ) is present before the accumulation of histopathological hallmarks of the disease. This scenario produces impaired functioning of neuronal networks, altered patterns of synchronous activity and...

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Veröffentlicht in:	PloS one 2015-07, Vol.10 (7), p.e0134385
Hauptverfasser:	Mayordomo-Cava, Jennifer, Yajeya, Javier, Navarro-López, Juan D, Jiménez-Díaz, Lydia
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer's disease Amyloid beta-Peptides - pharmacology Animal cognition Animal models Animals Channels Circuit design Conductance Excitability G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics Gene expression Gene Expression Regulation - drug effects Genes Glutamic acid receptors (metabotropic) Hippocampus Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology KCNQ Potassium Channels - genetics KCNQ2 protein Laboratory animals Learning Memory Molecular modelling Neural networks Neurodegenerative diseases Neurotransmission Neurotransmitter receptors Pathogenesis Peptide Fragments - pharmacology Polymerase chain reaction Potassium Potassium channels Potassium channels (inwardly-rectifying) Potassium channels (voltage-gated) Proteins Rats Rats, Wistar Real-Time Polymerase Chain Reaction Receptors Resistance Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA-directed DNA polymerase Rodents Transcription γ-Aminobutyric acid B receptors
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