Single and combined effects of carbamazepine and vinpocetine on depolarization-induced changes in Na+, Ca2+ and glutamate release in hippocampal isolated nerve endings

Effects of Vinpocetine on mitochondrial function and neuroprotection in primary cortical neurons

“…Table 1). ] i changes (Tretter and Adam-Vizi, 1998;Zelles et al, 2001;Sitges et al, 2006). Importantly, Vinpocetine did not influence the amplitude of the initial glutamate-evoked [Ca 2+ ] i rise indicating that Vinpocetine acts at least partially by influencing mechanisms controlling elevated [Ca 2+ ] i levels.…”

“…Vinpocetine can block phosphodiesterase I, which can be important for improvement of cerebral circulation (Pelligrino and Wang, 1998) and can act as an antioxidant . Vinpocetine also blocks voltage-gated sodium channels (VDSCs) in therapeutically relevant concentrations (<50 mM), decreases the Ca 2+ influx evoked by VDSC stimulation and can also attenuate Ca 2+ -dependent destructive processes (Lakics et al, 1995;Tretter and Adam-Vizi, 1998;Sitges and Nekrassov, 1999;Zelles et al, 2001;Sitges et al, 2006). Table 1). ]…”

“…We also used the forward side scatter (FSC) intensity, which roughly equals to the particle's size and can also be used to distinguish between cellular debris and living cells (see Fig. 4a (Tretter and Adam-Vizi, 1998;Sitges and Nekrassov, 1999;Zelles et al, 2001;Sitges et al, 2006). To test whether Vinpocetine can activate similar mechanisms during glutamate-induced excitotoxicity, ratiometric Fura-2 Ca 2+ imaging was performed in embryonal cortical neuronal cultures 6 days after plating (Fig.…”

Antiepileptic Drugs Targeting Cerebral Presynaptic Ion Channels Reduce Cerebral Excitability Decreasing Glutamate Release

“…Vinpocetine (ethyl apovincamine-22-oate) is a nootropic drug with neuroprotective capabilities discovered during the late 1960s that in animal models of hypoxia and ischemia exerts beneficial effects against neuronal damage and has been used in the treatment of central nervous system disorders of cerebral-vascular origin for decades. In brain isolated nerve endings vinpocetine inhibited the rise in the internal concentration of Na + and neurotransmitter release induced by veratridine (Tretter & Adam-Vizi, 1998;Sitges & Nekrassov, 1999;Trejo et al, 2001;Sitges et al, 2006), as well as the tetrodotoxin sensitive fraction of the rise in Na + and Ca 2+ induced by 4-aminopyridine . In hippocampus isolated nerve endings, vinpocetine inhibited glutamate release induced by increasing presynaptic Na + channels permeability with veratridine and by increasing presynaptic Ca 2+ channels permeability with high K + in a much lower range of concentrations than carbamazepine, phenytoin, lamotrigine and oxcarbazepine (Sitges et al, 2007a;2007b).…”

Characterization of Phenytoin, Carbamazepine, Vinpocetine and Clorgyline Simultaneous Effects on Sodium Channels and Catecholamine Metabolism in Rat Striatal Nerve Endings

“…In hippocampal synaptosomes preloaded with radioactive Glu ([ 3 H]Glu) several of the most amply used antiepileptic drugs and the new potential antiepileptic vinpocetine (ethyl apovincamine-22-oate) inhibited [ 3 H]Glu release induced by veratridine in the absence of external Ca 2+ ; vinpocetine being the most potent [6,7]. Also in the guinea pig in vivo phenytoin and carbamazepine were less potent than vinpocetine to inhibit the epileptic cortical activity induced by the convulsing agent, pentylenetetrazole [8].…”