Summary
3H-Noradrenaline release in the rabbit hippocampus and its possible modulation via presynaptic dopamine receptors was studied. Hippocampal slices were preincubated with 3H-noradrenaline, continuously superfused in the presence of cocaine (30 μmol/l) and subjected to electrical field stimulation. The electrically evoked tritium over-flow from the slices was reduced by 0.1 and 1 μmol/l dopamine and apomorphine, but significantly enhanced by 10 μmol/l apomorphine or by 0.1 and 1 μmol/l bromocriptine. If the α2-adrenoceptor antagonist yohimbine (0.1 μmol/l) was present throughout superfusion, the inhibitory effects of dopamine and apomorphine were more pronounced and even 10 μmol/l apomorphine and 1 μmol/l bromocriptine inhibited noradrenaline release. Qualitatively similar observations were made in the presence of another α2-antagonist, idazoxane (0.1 μmol/l). In the presence of the D2-receptor antagonist domperidone (0.1 μmol/l) the inhibitory effects of dopamine were almost abolished, whereas both apomorphine (>1 μmol/l) and bromocriptine (>0.01 μmol/l) greatly facilitated noradrenaline release. The D2-receptor agonist LY 171555 (0.1 and 1 μmol/l) significantly reduced the evoked noradrenaline release whereas the D1-selective agonist SK & F 38393 was ineffective at similar concentrations. The effects of LY 171555 were abolished in the presence of domperidone (0.1 μmol/l) but remained unchanged in the presence of yohimbine or idazoxane (0.1 μmol/l, each).
At 1 μmol/l the D2-receptor antagonists domperidone and (-)sulpiride significantly increased the evoked noradrenaline release by about 10%. However, at this concentration, domperidone (but not (-)sulpiride) affected also basal tritium outflow. Bulbocapnine and the preferential D1-receptor antagonists SCH 23390 enhanced the evoked noradrenaline release already at 0.1 μmol/l. Their marked facilitatory effects (50 to 60% increase at 1 μmol/l) were reduced in the presence of idazoxane (0.1 μmol/l) and almost abolished in the presence of 0.1 μmol/l yohimbine, whereas the increase due to 1 μmol/l (-)sulpiride persisted under these conditions.
The evoked tritium efflux from rabbit hippocampal slices preincubated with 3H-serotonin was not affected by dopamine receptor agonists.
From our results we conclude that hippocampal noradrenaline, but not serotonin release, is modulated via D2-dopamine receptors. In addition, our results provide evidence for more or less pronounced α2-adrenoceptor agonistic properties of dopamine and α2-adrenoceptor antagonistic properties of apomorphine, bromocriptine, SCH 23390 and bulbocapnine in this noradrenaline release model from CNS tissue.
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Jackisch, R., Moll, S., Feuerstein, T.J. et al. Dopaminergic modulation of hippocampal noradrenaline release. Naunyn-Schmiedeberg's Arch. Pharmacol. 330, 105–113 (1985). https://doi.org/10.1007/BF00499902
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DOI: https://doi.org/10.1007/BF00499902