Abstract
Portal-systemic encephalopathy (PSE) is associated with increased brain turnover of serotonin (5-hydroxytryptamine; 5-HT). Despite this metabolic increase, neuronal release of 5-HT is unaltered in neocortex of portacaval shunted (PCS) rats. In the present study, frontal neocortical extracellular 5-HT and 5-hydroxyindole-3-acetic acid (5-HIAA) levels were determined in PCS rats and sham-operated controls prior to, as well as, after acute challenge with L-tryptophan (L-TRP; a bolus dose of 280 mg/kg i.p. followed by 5 consecutive hourly doses of 50 mg/kg). Neither basal 5-HT nor 5-HIAA extracellular levels were significantly altered in PCS rats compared to controls. L-TRP administration resulted in unaltered extracellular 5-HT but elevated 5-HIAA levels in PCS and sham rats. These findings do not suggest that changes in brain neuronal 5-HT release play any major functional role in the pathogenesis of chronic PSE. The present data also emphasize the importance of distinguishing between brain 5-HT metabolism and brain 5-HT release.
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