Diet induced hyperammonemia decreases neuronal nuclear size in rat entorhinal cortex.

Hepatic encephalopathy is mainly caused by an excess of ammonium ions. Among other effects, glutamate transmission in the brain is impaired, and thereof, neuronal function in multiple systems is affected. We investigated in rats the effect of diet induced hyperammonemia in the entorhinal cortex, a well known glutamatergic pathway to the dentate gyrus, by measuring the neuronal nuclear area in two entorhinal cortex subfields (dorsolateral subfield (DLE) and dorsal intermediate subfield (DIE); [Insausti, R., Herrero, M.T. and Witter, M.P., Origin and distribution of cortical efferents from the entorhinal cortex in the rat, Hippocampus, 7 (1997) 146-183]) that project to separate septotemporal levels of the hippocampus. After 2, and more overtly, after 8 weeks of the ammonium enriched diet consumption, the neuronal nuclear size in layers II, III, V and VI of both entorhinal cortex subfields showed a significant reduction in size. We conclude that already at 2 weeks of treatment there is a decrease in neuronal nuclear size in all layers of the entorhinal cortex, which might have widespread functional effects on cortical and subcortical structures.