Vinpocetine facilitates noradrenaline release in rat brain cortex slices

Abstract

Schlicker, E., R. Betz and M. Gothert: Vinpocetine facilitates noradrenaline release in rat brain cortex slices. Drug Dev. Res. 14:285-291, 1988. Rat brain cortex slices preincubated with ,H-noradrenaline were superfused with physiological salt solution, and the effect of vinpocetine on the electrically (3 Hz) evoked overflow was studied. Vinpocetine at 10-1 00 pmoliliter facilitated the evoked overflow: at 32 and 100 pmoliliter, 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 ([3a-tropanyll-1 H-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 pmoliliter. The present results show that vinpocetine facilitates noradrenaline release. This effect may be related to the blockade of presynaptic a,-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.

Structural requirement of the calcium-channel subunit α2δ for gabapentin binding

“…Although both sets of data are consistent in pointing to the importance of these flanking regions, it remains to be determined which amino acids in region H may play key roles for gabapentin binding as well as for Ca# +channel-mediated dopamine release. The overlapping structural requirements for α # δ-involved dopamine release and gabapentin binding may provide a link between gabapentin-attenuated monoamine release [32,33] and Ca# + -channel function. Although one previous study failed to show any significant effect of gabapentin on the L-, N-or T-type voltage-dependent Ca# + channels [34], a recent study showed that gabapentin inhibits Ca# + currents mediated by the L-type Ca# + channel in isolated rat-brain neurons [35].…”

Nauclea latifolia stem-bark extract protects the prefrontal cortex from valproic acid - induced oxidative stress in rats: Effect on B-cell lymphoma and neuron specific enolase protein expression

“…The mechanism by which vinpocetine enhances spatial memory is thought to be by modulation of cholinergic functions specifically increasing firing rate of certain cells in the cholinergic pathway [39]. Several mechanisms involved in vinpocetine improvement of memory deficit and blood flow include inhibition of phosphodiesterase enzyme (PDE) enhancing second messenger signaling; inhibition of kB kinase (IKK)/ nuclear factor -kappa (NF -kB) and extracellular signal related kinase (ERK) reducing the inflammatory responses in vascular smooth muscle; and enhancing the structure of dendritic spines improving memory retrieval in mild to moderate psychodromes and cognitive enhancement.…”