The effects of serotonin depletion on the voltammetric response to amphetamine.

In vivo voltammetry with carbon paste electrodes reliably produces two oxidation peaks. Previous research suggests that in caudate peak 1 (P1) monitors ascorbic acid and peak 2 (P2) monitors uric acid. To provide additional evidence that P2 monitors uric acid rather than indoles, the effects of the serotonin synthesis inhibitor p-chlorophenylalanine (PCPA) were studied in caudate (serotonin-poor) and globus pallidus (serotonin-rich). In both caudate and globus pallidus PCPA had little effect on P2 and pretreatment with PCPA failed to inhibit the amphetamine-induced increase in P2. In general, P2 recorded from globus pallidus was always very similar to P2 recorded from caudate. These data are consistent with the hypothesis that P2 represents uric acid even in serotonin-rich areas of the brain. Pretreatment with PCPA dramatically enhanced the amphetamine-induced increase in P1 in caudate but not in globus pallidus. This finding is interesting in light of reports that PCPA enhances certain behavioral effects of amphetamine.