Vinpocetine facilitates noradrenaline release in rat brain cortex slices

Abstract

AbstractRat brain cortex slices preincubated with 3H‐noradrenaline were superfused with physiological salt solution, and the effect of vinpocetine on the electrically (3 Hz) evoked 3H overflow was studied. Vinpocetine at 10–100 μmol/liter facilitated the evoked overflow; at 32 and 100 μmol/liter, basal efflux was slightly increased. The facilitatory effect of vinpocetine on the evoked overflow was not altered by desipramine, rolipram (an inhibitor of cAMP phosphodiesterase), or ICS 205‐930 ([3α‐tropanyl]‐1H‐indole‐3‐carboxylic acid ester; an antagonist at 5‐HT3 (M) receptors); it was strongly attenuated by phentolamine. In turn, vinpocetine moderately decreased the facilitatory effect of phentolamine on the evoked overflow. The concentrationresponse curve of noradrenaline (obtained in the presence of desipramine) for its inhibitory effect on the evoked overflow was not shifted to the right by vinpocetine at 32 and 100 μmol/liter. The present results show that vinpocetine facilitates noradrenaline release. This effect may be related to the blockade of presynaptic α2‐adrenoceptors (although evidence is not unequivocal), but does not appear to involve inhibition of noradrenaline uptake or cAMP phosphodiesterase nor activation of 5‐HT3 (M) receptors. The facilitatory effect of vinpocetine on noradrenaline release occurs at concentrations higher than those obtained under treatment with this drug.