Portal-systemic encephalopathy (PSE) is associated with an increased brain tissue turnover of serotonin (5-HT). Despite increased 5-HT metabolism, brain 5-HT release in rats with a portacaval shunt (PCS) seems to be unaltered. Although this may indicate that the overall 5-HT output is unaltered in PSE, it is also possible that the 5-HT release pattern might be altered in some way. In the present study, the potassium-evoked frontal neocortical release of 5-HT was studied in experimental chronic PSE. KCI (60 mM) produced marked increases in the 5-HT output compared with basal values both in PCS and sham rats. Simultaneously, the KCI challenge resulted in significant elevations in the 5-HT release of PCS compared with sham. In Ca2+-free medium, the difference between PCS and sham rats in the KCl-evoked release of 5-HT was abolished. In the presence of TTX (1 mM), both groups displayed increased extracellular 5-HT levels. Again, a difference with higher amplitude of the 5-HT release in PCS compared with sham was evident. It is concluded that in experimental chronic PSE an augmented neocortical 5-HT release compared with the normal in vivo situation is available. The possible mechanism(s) responsible for the difference in neocortical 5-HT output between PCS and sham-operated rats in response to the KCl-challenge is discussed.
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