Interleukin‐2 Modulates Evoked Release of [3H]Dopamine in Rat Cultured Mesencephalic Cells

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Abstract
Mesencephalic cell cultures were used as a model to investigate the effects of interleukin‐2 (IL‐2) on evoked release of [3H]dopamine ([3H]DA) and γ‐[3H]‐aminobutyric acid ([3H]GABA). At low concentrations (10−13‐10−12M), IL‐2 potentiated [3H]DA release evoked by the excitatory amino acids N‐methyl‐D‐aspartate (NMDA) and kainate, whereas higher IL‐2 concentrations (10−9‐10−8M) had no effect. IL‐2 (10−14‐10−8M) modulated K+‐evoked [3H]DA release in a biphasic manner, with low concentrations (10−12‐10−11M) of IL‐2 potentiating and higher concentrations (10−9‐10−8M) inhibiting K+‐induced [3H]DA release. IL‐2 (10−14‐10−8M) by itself failed to alter spontaneous [3H]DA release. The inhibition by IL‐2 of K+‐evoked [3H]DA release was reversible and not due to neurotoxicity, as preexposure to IL‐2 (10−8M) had no significant effect on the subsequent ability of dopaminergic cells to take up and to release [3H]DA. Under our experimental conditions, IL‐2 (10−8 M) did not alter Ca2+‐independent [3H]GABA release evoked by either K+ or NMDA. The results of this study indicate that IL‐2 is able to potentiate [3H]DA release evoked by a number of different stimuli, including K+ depolarization and activation of both NMDA and non‐NMDA receptor subtypes in mesencephalic cell cultures. IL‐2 is active at very low concentrations, a finding that indicates a potent effect of IL‐2 on dopaminergic neurons and implicates a physiological role for this cytokine in the modulation of DA release.