Author/Authors :
Babri، Shirin نويسنده Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran , , Amani، Mohammad نويسنده Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran , , Mohaddes، Gisou نويسنده Department of Physiology, Tabriz University of Medical Sciences, Tabriz, IR Iran , , Alihemmati، Alireza نويسنده Department of Histology & Embryology, Tabriz University of Medical Sciences, Tabriz, Iran. , , Ebrahimi، Hadi نويسنده Department of Physiology, Tabriz University of Medical Sciences, Tabriz, IR Iran ,
Abstract :
Introduction: Alzheimer’s disease (AD) is a common neurodegenerative disorder in elderly people with an impairment of cognitive decline and memory loss. B-amyloid (AB) as a potent neurotoxic peptide has a pivotal role in the pathogenesis of AD. This disease begins with impairment in synaptic functions before developing into later neuro-degeneration and neuronal loss. The aim of this study was to evaluate the synaptic plasticity and electrophysiological function of granule cells in hippocampal dentate gyrus (DG) after intracerebroventricular (i.c.v.) administration of aggregated AB (1-42) peptide in vivo. Methods: Animals were divided to control and AB (1-42) groups. Long-term potentiation (LTP) in perforant path-DG synapses was assessed in order to investigate the effect of aggregated AB (1-42) on synaptic plasticity. Field excitatory post-synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured. Results: Administration of AB (1-42) significantly decreased fEPSP slope and PS amplitude in AB (1-42) group comparing with the control group and had no effect on baseline activity of neurons. Conclusion: The present study indicates that administration of aggregated form of AB (1-42) into the lateral ventricle effectively inhibits LTP in granular cells of the DG in hippocampus in vivo.
