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In Vivo Mechanisms Underlying Dopamine Release from Rat Nigrostriatal Terminals: II. Studies Using Potassium and Tyramine

Abstract: The brain microdialysis technique has been used to examine the in vivo effects of potassium and tyramine on dopamine (DA) release and metabolism in the striatum of halothane‐anaesthetised rats. Increasing the concentration of potassium perfusing the dialysis probe (30–120 mM) induced a dose‐related efflux of DA. A dose‐related release of DA was also observed following addition of tyramine (1–100 μM) to the perfusing buffer. High concentrations of potassium were found to reduce the dialysate content of the DA metabolites 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid and the serotonin metabolite 5‐hydroxyindoleacetic acid. No such effect was observed even when using the highest concentration of tyramine tested. Potassium‐evoked DA release was facilitated by pretreatment with the DA uptake inhibitor nomifensine, was inhibited by depletion of extracellular calcium, and was not significantly affected by tetrodotoxin (TTX). The effect of tyramine on DA efflux was inhibited by nomifensine and was insensitive to both TTX and calcium depletion. These data suggest that potassium and tyramine induce release of DA via different mechanisms. Potassium‐induced DA release involves a carrier‐independent process and may utilise an exocytotic release mechanism. On the other hand, tyramine‐induced DA release would appear to involve a carrier‐dependent process. Depletion of vesicular stores of DA by pretreatment with reserpine did not significantly affect potassium‐induced DA release, whereas a marked inhibition of the effects of tyramine was noted. However, in reserpinised animals the potassium‐induced release of DA was inhibited by nomifensine, a result suggesting that a carrier‐dependent release mechanism operates in the absence of vesicular DA. Inhibition of DA synthesis by pretreatment with α‐methyl‐p‐tyrosine (α‐MPT) reduced potassium‐evoked DA release. However, this treatment only impaired the effect of tyramine when α‐MPT was given 120 min before tyramine, when vesicular DA stores are also depleted. These data suggest that tyramine induces release of DA from vesicular stores, whereas the effect of potassium involves newly synthesised DA. Because DA metabolite levels are reduced by potassium but not by tyramine, these data suggest that extracellular DOPAC is derived from a newly synthesised pool(s) of DA.