Table of Contents
International Journal of Peptides
Volume 2013, Article ID 328140, 11 pages
Research Article

Amyloid Beta Peptides Differentially Affect Hippocampal Theta Rhythms In Vitro

1Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, UNAM, Boulevard Juriquilla 3001, 16230 Querétaro, Mexico
2Departamento de Farmacobiología, Cinvestav-IPN, Calzada de los Tenorios 235, Col. Granjas Coapa, 14330 México, DF, Mexico

Received 24 March 2013; Accepted 3 June 2013

Academic Editor: John D. Wade

Copyright © 2013 Armando I. Gutiérrez-Lerma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Soluble amyloid beta peptide (Aβ) is responsible for the early cognitive dysfunction observed in Alzheimer's disease. Both cholinergically and glutamatergically induced hippocampal theta rhythms are related to learning and memory, spatial navigation, and spatial memory. However, these two types of theta rhythms are not identical; they are associated with different behaviors and can be differentially modulated by diverse experimental conditions. Therefore, in this study, we aimed to investigate whether or not application of soluble Aβ alters the two types of theta frequency oscillatory network activity generated in rat hippocampal slices by application of the cholinergic and glutamatergic agonists carbachol or DHPG, respectively. Due to previous evidence that oscillatory activity can be differentially affected by different Aβ peptides, we also compared and for their effects on theta rhythms in vitro at similar concentrations (0.5 to 1.0 μM). We found that reduces, with less potency than , carbachol-induced population theta oscillatory activity. In contrast, DHPG-induced oscillatory activity was not affected by a high concentration of but was reduced by . Our results support the idea that different amyloid peptides might alter specific cellular mechanisms related to the generation of specific neuronal network activities, instead of exerting a generalized inhibitory effect on neuronal network function.