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Introduction: Alzheimer's disease (AD) is a common neurodegenerative disorder in elderly people with an impairment of cognitive decline and memory loss. β-amyloid (Aβ) 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 intracere broventricular (i.c.v.) administration of aggregated Aβ (1-42) peptide in vivo. Methods: Animals were divided to control and Aβ (1-42) groups. Long-term potentiation (LTP) in perforant path-DG synapses was assessed in order to investigate the effect of aggregated Aβ (1-42) on synaptic plasticity. Field excitatory post-synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured. Results: Administration of Aβ (1-42) significantly decreased fEPSP slope and PS amplitude in Aβ (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 Aβ (1-42) into the lateral ventricle effectively inhibits LTP in granular cells of the DG in hippocampus in vivo. [ABSTRACT FROM AUTHOR]