Effects of single and continuous administration of amyloid ß-peptide (25-35) on adenylyl cyclase activity and the somatostatinergic system in the rat frontal and parietal cortex
Autores
Hervás Aguilar, América; Puebla Jiménez, LilianIdentificadores
Enlace permanente (URI): http://hdl.handle.net/10017/2374DOI: 10.1016/j.neuroscience.2005.02.017
ISSN: 0306-4522
Editor
Nature Publishing Group
Fecha de publicación
2005Cita bibliográfica
Neuroscience, 2005, v. 135, n. 1, p. 181–190
Palabras clave
Brain
Alzheimer's disease
Somatostatin receptors
Cerebral cortex
Proyectos
PM99-0129 (Ministerio de Ciencia y Tecnología)
Tipo de documento
info:eu-repo/semantics/article
Versión
info:eu-repo/semantics/publishedVersion
Versión del editor
http://dx.doi.org/10.1016/j.neuroscience.2005.02.017Derechos
© Elsevier, 2005
Derechos de acceso
info:eu-repo/semantics/openAccess
Resumen
It is unknown whether the amyloid β-peptide (Aβ), a principal component found in extracellular neuritic plaques in the brain of patients with Alzheimer’s disease (AD), is capable of altering adenylyl cyclase (AC) activity and the somatostatin (SRIF) receptor-effector system in the cerebral cortex of the patients. Therefore, the objective of this study was to investigate the effect of the β fragment, β (25–35), on AC activity and the somatostatinergic system in the rat frontoparietal cortex. A single dose of β (25–35) (10μg) injected intracerebroventricularly significantly decreased the density of SRIF receptors (27.4%) and increased their affinity (32.2%) in the frontoparietal cortex. The inhibitory effect of SRIF on basal and forskolin (FK)-stimulated AC activity was significantly lower in the β (25–35)-treated rats when compared with controls. β (25–35) did not modify Giα1, Giα2 nor Giα3 levels in membranes from the frontoparietal cortex. Continuous infusion of the peptide induced a decrease in the SRIF receptor density in this brain area to a similar extent as that observed 14 days after the single administration of the peptide. Likewise, this treatment decreased the SRIF receptor density in the frontal cortex (15.3%) and parietal cortex (27.2%). This effect was accompanied by a decrease in the SRIF-mediated inhibition of FK-stimulated AC activity (from 41.6% to 25.6%) in the frontal cortex as well by a decrease in basal AC activity (from 36.9% to 31.6%) and FK-stimulated AC activity (from 35.6% to 27.1%) in the parietal cortex. Continuous infusion of Aβ (25–35) had no effect on Giα1, Giα2 or Giα3 levels in membranes from frontal and parietal cortex. However, this treatment caused a decrease in SRIF-like immunoreactivity content in the parietal (38.9%) and frontal (20.4%) cortex. These results suggest that Aβ might be involved in the alterations of somatostatinergic system reported in AD.
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EFFECTS OF SINGLE....pdf | 332.8Kb |
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