Abstract
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. Two groups of control rats recieved either water as vehicle (Con) or probitics (Pro + Con). Also 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 in the Pro + Alz rats. 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.
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