Reduced cortical excitability and synaptic proteins in the brain of ApoE deficient mice

Apolipoprotein E (ApoE) is the major glycoprotein in the brain and plays a critical role in the transport of cholesterol and other lipids. Besides, ApoE has a crucial function in the maintenance of synaptodendritic connections, and repair of neurons. ApoE knockout (ApoE-KO) mice model whose apoE gene has been knocked out has great importance for understanding the effect of ApoE and loss of function of ApoE. Scientists have reported cognitive impairment in ApoE-KO mice, with cholinergic deficits, decreased synaptic excitability. In the present study, we investigated the difference between the basal cortical electrical activity of ApoE-KO and that of wild type (WT) mice. We also measured the neuroinflammatory markers (TNF-α, IL-6) and synaptic proteins (synaptophysin and PSD-95) in the cortex and the hippocampus. Electrocorticography (ECOG) of the mice were recorded and then animals were sacrificed. Brains were removed and biochemical analysis was performed in the cortex and hippocampus tissues by using ELISA. The result of the ECOG power analysis revealed that the power of the basal electrical activity was significantly smaller in ApoE-KO mice than WT controls. Biochemical analysis showed that in ApoE-KO mice, PSD-95 and synaptophysin levels were significantly lower than WT controls. Neuroinflammation markers, TNF-α and IL-6, were not different between groups. As a conclusion, ApoE deficient mice have suppressed cortical excitability and reduced synaptic proteins in the cortex and in the hippocampus. The findings may help understanding the relation between ApoE and neuronal function.