Effects of pharmacological agents, sleep deprivation, hypoxia and transcranial magnetic stimulation on electroencephalographic rhythms in rodents: Towards translational challenge models for drug discovery in Alzheimer’s disease
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Otros documentos de la autoría: Babiloni, Claudio; Infarinato, Francesco; Aujard, Fabienne; Bastlund, Jesper Frank; Bentivoglio, Marina; Bertini, Giuseppe; Del Percio, Claudio; Fabene, Paolo Francesco; Forloni, GianLuigi; Herrero Ezquerro, María Trinidad; Noè, Francesco Mattia; Pifferi, Fabien; Ros Bernal, Francisco; Christensen, Ditte Zerlang; Dix, Sophie; Richardson, Jill C.; Lamberty, Yves; Drinkenburg, Wilhelmus; Rossini, Paolo Maria
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Metadatos
Título
Effects of pharmacological agents, sleep deprivation, hypoxia and transcranial magnetic stimulation on electroencephalographic rhythms in rodents: Towards translational challenge models for drug discovery in Alzheimer’s diseaseAutoría
Fecha de publicación
2013Editor
ElsevierISSN
1388-2457; 1872-8952Cita bibliográfica
Clinical Neurophysiology Volume 124, Issue 3, March 2013, Pages 437–451Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
http://www.sciencedirect.com/science/article/pii/S1388245712005810Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
Different kinds of challenge can alter spontaneous ongoing electroencephalographic (EEG) rhythms in animal models, thus providing paradigms to evaluate treatment effects in drug discovery. The effects of challenges ... [+]
Different kinds of challenge can alter spontaneous ongoing electroencephalographic (EEG) rhythms in animal models, thus providing paradigms to evaluate treatment effects in drug discovery. The effects of challenges represented by pharmacological agents, hypoxia, sleep deprivation and transcranial magnetic stimulation (TMS) on EEG rhythms are here reviewed to build a knowledge platform for innovative translational models for drug discovery in Alzheimer’s disease (AD). It has been reported that antagonists of cholinergic neurotransmission cause synchronisation of spontaneous ongoing EEG rhythms in terms of enhanced power of EEG low frequencies and decreased power of EEG high frequencies. Acetylcholinesterase inhibitors and serotonergic drugs may restore a normal pattern of EEG desynchronisation. Sleep deprivation and hypoxia challenges have also been reported to elicit abnormal synchronisation of spontaneous ongoing EEG rhythms in rodents. The feasibility and reproducibility of TMS have been demonstrated in rodents but information on a consistent modulation of EEG after TMS manipulation is very limited. Transgenic mice over-expressing human amyloid precursor protein complementary DNAs (cDNAs) harbouring the ‘Swedish’ mutation and PS-1 cDNAs harbouring the A264E mutation, which recapitulate some of the pathological features of AD, exhibit alterations of spontaneous ongoing EEG rhythms at several low and high frequencies. This does not appear, however, to be a consequence of beta-amyloid deposition in the brain. The present review provides a critical evaluation of changes of spontaneous ongoing EEG rhythms due to the experimental manipulations described above, in order to stimulate the promote more adherent models fitting dynamics in humans. [-]
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Clinical Neurophysiology, 2013, Vol. 124, Num. 3Derechos de acceso
Copyright © 2012 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.this is the author’s version of a work that was accepted for publication in Clinical Neurophysiology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Clinical Neurophysiology, VOL 124, ISSUE 3, (2013) DOIhttp://dx.doi.org/10.1016/j.clinph.2012.07.023
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