It has been postulated that excess ammonia and neuroinflammation resulting from liver failure induces astrocytic swelling which can lead to increased BBB permeability and neuronal dysfunction. The impacts of high levels of blood ammonia on the brain energy metabolism is not clear. The objective of current study is to evaluate the neurotransmitter metabolism in CCl4 induced liver injury mouse model using using 1H-[13C]-NMR spectroscopy together with [1,6-13C2]glucose infusion. Our findings indicate reduction in the activity of glutamatergic and GABAergic neurons in the chronic liver damage condition.
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