An HPLC anaIysis of the endogenous amine levels in pooled fractions under conditions of basal release, as well as calcium and 5 HT evoked release conditions, showed that the increase in tritium efflux is accompanied by a large increase in DA re acrease in 3 d yd np b ished observa T enhanced DA efflux he reuptake of spontauld result in a net increase in the basal release of this amine, can also be ruled out since if this had been the case the .5 HT indueed release of tritium would not have been prevented by DA uptake blockers. ? difference be the paradigm used na et al. to the stimulatory effect gtf S HT is that these investigators used striatal sjices. while striatal synaptosomes were used in this study. Thus, it is possible that the stimulatory effects obsrn ed in slices were not mediated by receptors on DA nerve terminals but by receptors on i terneurons or on other terminals, such as those of the corticostriatal gl tam ner c pathway for example. In support of interneuron involvement, Blandina et al. 11989 reported that the stimulatory effect of S I IT was reduced 40 by t trodotoxi . Another difference behveen the present study and that of land na et al.
is that in the latter nomifensine was included in all experiments. Since n mifens n blocked the S HT enhanced release in the experiments reported here, this further suggests that the 5 W induced Tivantinib selleckchem release observed by al. did not involve the same meshat observed in striatal synaptosomes in this study. te est ng y, Schmidt and Black reported that triti m efflus was increased by the S HT, agonist, phenylbiguanide, and this increase was blocked by nomifensine, but not by the WIT, antagonists KS 5. 3 or MDL 73.137. These results suggest that, like S ST. e y bi anide also induces DA release by an interaction with the DA uptake carrier. Another significant difference between this study and that of Blandina et al. is that the present work was done by measuring release of newly taken up A. while Blandina et al. monitored endogenous DA release. However, f H DA released by either depolarization or arnp t nine has been found to closely mimic endogenous DA ease, although there are some quantitative differences in the two measures QHerdon et al 1985 .
Furthermore, our own relirni a studies showed that cocaine blocked the release of endagenous DA evoked by 5 HT and calcium. Thus, it buy Nilotinib seems unlikely that the measurement of I?HIDA, rather than endogenous DA, could account for the discrepancy between this study and that of land a et al Apart from its action in increasing basal tritium T also caused an approximate fold increase in the calcium evoked release of tritium. In contrast, d LSD had no effect on stimulated tritium release. As with the increase in basal tritium efflux by j HT. the action of 5 HT on calcium evoked tritium release was prevented by the uptake inhibitors cocaine and nomifensine.