Studies demonstrate that damage to gut microbiota is associated with some brain disorders including neurodegenerative diseases such as Alzheimer's disease (AD). Accordingly, supporting gut microbiota has been considered as a possible strategy for AD treatment. We evaluated behavioral and electrophysiological aspects of the brain function in an animal model of AD made by intracerebroventricular injection of β-amyloid. The Con and Pro + Con rats received vehicle and probiotics, respectively. Two groups of Alzheimeric animals were treated by either vehicle (Alz) or probiotics (Pro + Alz). Sham group was only subjected to surgical procedure and received the vehicle. Spatial learning and memory was assessed in Morris water maze. Also, basic synaptic transmission and long-term potentiation (LTP) were assessed by recording field excitatory postsynaptic potentials (fEPSPs) in hippocampus. Change in anti-oxidant/oxidant factors was assessed via measuring plasma level of total anti-oxidant capacity (TAC) and malondealdehyde (MDA). Brain staining was done to confirm β-amyloid accumulation. Fecal bacteria quantification was accomplished to find how probiotic supplement affected gut microbiota. We found that while the Alz animals displayed a weak spatial performance, probiotic treatment improved the maze navigation. Whereas basic synaptic transmission remained unchanged in the Alz rats, LTP was suppressed in this group. Probiotic treatment significantly restored LTP in the Pro + Alz group and further enhanced it in the Pro + Con rats. The intervention also showed a favorable effect on balance of the anti-oxidant/oxidant biomarkers in the Pro + Alz rats. This study provides the first proof on positive effect of probiotics on synaptic plasticity in an animal model of AD.