Endogenous dopamine release from tuberoinfundibular neurons: does calmodulin play any role?

Naunyn-Schmiedeberg's Archives of Pharmacology
G Di RenzoL Annunziato

Abstract

The possible involvement of calmodulin in the process of endogenous dopamine (DA) release from arcuate-periventricular nuclei-median eminence fragments, containing tuberoinfundibular dopaminergic (TIDA) neurons, has been investigated in an in vitro incubation system. For this purpose the basal and K+-stimulated DA release was examined in the presence and in the absence of the different putative calmodulin antagonists, pimozide, trifluoperazine, penfluridol and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). Trifluoperazine and pimozide in concentrations up to 100 microM were both uneffective in blocking K+-evoked DA release. Penfluridol in doses of 5 and 10 microM, did not prevent 35 mM K+-induced endogenous DA release. It was able to reduce K+-stimulated DA release only at the very large concentration of 100 microM. W-7 added in vitro to the hypothalamic fragments, prevented endogenous DA release evoked by 35 mM K+ in a dose-dependent manner. W-5, a chlorine deficient analogue of W-7, that interacts only weakly with calmodulin, failed to modify K+-stimulated endogenous DA release in doses up to 200 microM. All the putative calmodulin antagonists used in the present study did not induce any change of basal DA release....Continue Reading

References

Sep 1, 1980·The Journal of Clinical Investigation·Y KrauszG W Sharp
Jul 23, 1984·Life Sciences·L AnnunziatoA Quattrone
Jul 1, 1981·Proceedings of the National Academy of Sciences of the United States of America·H HidakaT Nagata

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