REVIEW Vinpocetine, a semisynthetic derivative of Vincamine alkaloid, extracted from the periwinkle (plant) Vinca minor, is the first full-fledged nootropic (a supplement possibly affecting the mind). Tested as a neuronal plasticity enhancer, marketed as a ''memory booster'', vinpocetine has been shown to facilitate long-term potentiation, improve spatial memory in animal models, and enhance performance on cognitive tests in humans. Vinpocetine has several pharmacological and biochemical actions, including stimulating cerebral vasodilation, increasing tolerance of cerebral tissue to hypoxic and ischemic insults, anticonvulsant activity, inhibitory effects on phosphodiesterase (PDE), improving hematological flow properties and inhibiting thrombocyte aggregation. The cognitive enhancement function of vinpocetine comes from its inhibition of PDE type 1, which leads to an increase in cAMP and cGMP levels. These cyclic nucleotides can in turn activate a series of kinases that phosphorylate the transcription factors cAMP response element binding protein (CREB) and serum response factor (SRF), leading to the expression of plasticity- related genes. Recently, it has been shown that vinpocetine inhibits IKK, preventing I-kappaB degradation and the consequent translocation of NF-kappaB to the nucleus, and is independent of vinpocetine action on PDE1.
Vinpocetine also appears to provide direct neuroprotective effects under in vitro and in vivo conditions. These effects appear to be related to the inhibition of voltage-dependent neuronal sodium channels, indirect inhibition of some molecular cascades initiated by the rise of intracellular calcium levels and to a lesser extent, inhibition of adenosine reuptake. These neuroprotective effects might also be enhanced by vinpocetine 's selective inhibition of calcium calmodulin-dependent cGMP-PDE. This inhibition may enhance intracellular cGMP levels in vascular smooth muscle, leading to reduced cerebrovascular resistance and increased cerebral blood flow.
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