Omega-3 fatty acids prevent LPS-induced passive avoidance learning and memory and CaMKII-α gene expression impairments in hippocampus of rat

Background: Neuroinflammation is considered to be a major factor in several neurodegenerative diseases. Recently, the polyunsaturated fatty acid omega-3 has been shown to have anti-inflammatory effects and might play an effective role in improving memory impairment due to inflammation. In order to test this, we stimulated neuroinflammation in an animal model and induced memory dysfunction as measured by reduced retention of passive avoidance learning (PAL) and altered expression of CaMKII-alpha, a gene known to be crucial for memory formation. We then investigated whether treatment with dietary omega-3 prevents inflammation-induced memory dysfunction in this model. Methods: Male wistar rats (200-220 g) were fed either a control diet or a diet containing omega-3 (400 mg/kg, po) for 1 month prior. Rats then received injection of either saline or LPS (500 mu g/kg, ip) and were subjected to the PAL acquisition task. The retention test was performed 24 h later, and animals were sacrificed immediately. Hippocampi were dissected and stored at -80 degrees C. Finally, TNF-alpha levels and CaMICII-alpha gene expression were measured by ELISA and qRT-PCR, respectively. Results: We found that LPS treatment significantly impaired PAL and memory, increased TNF-a levels and impaired CaMKII-alpha gene expression. In control and LPS-injected animals, pre-treatment with omega-3 improved performance on the PAL task and increased CAMKII-alpha gene expression. Conclusion: Taken together, these data suggest that dietary omega-3 may improve cognitive function and provide a potential therapy for memory impairment due to neuroinflammation. (C) 2014 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.