Hippocampal glutamate release after porta cava anastomosis: Reduced sensitivity to ammonia inhibition

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Abstract
In vitro measurements of basal efflux and evoked release of exogenous and endogenous glutamate from rat hippocampus showed that exposition of the tissue to pathophysiological concentrations of ammonium chloride (3 mM) for 40–60 min abolished the KC1‐induced release of endogenous glutamate. Basal efflux of endogenous glutamate was elevated by ammonium chloride with a delay of 30–40 min. In an attempt to link these observations to the pathogenesis of hepatic coma, rats were subjected to porta‐cava anastomosis, and the hippocampal tissue was tested for ammonia sensitivity 3–4 weeks after the operation. The results showed that ammonia perfusion of the tissue was without effect on either basal or KCl‐evoked release of endogenous glutamate. In addition, the utilization of glutamine for glutamate formation was influenced in hippocampal but not cortical tissue form porta‐cava anastomized rats. The results suggest that ammonia is an important factor for the disturbed metabolism of the neurotransmitter pool of glutamate in hepatic failure.