The Excitement of Vinpocetine
by Will Block

Almost thirty years ago, European pharmacognosy researchers coalesced around a substance naturally found in small amounts in different varieties of the periwinkle garden plant. Pharmacognosy is the study of the medical properties of plants. This periwinkle herbal extract, called vinpocetine, was examined for some of the traditional uses indicated by folklore healing regimens and anecdotal evidence. The idea was to research periwinkle's antique remedies to determine if any might have modern applications. Periwinkle was mentioned in the 1st Century scientific volumes De Materia Medica of Dioscorides.1 Once its mode of operation became clear, other lines of investigation grew. By the early 1970's, excitement was in the air as researchers reveled in the success of their findings. They found vinpocetine to be safe and non-toxic with an amazing array of functional and structural benefits for improved health. They also found a lot more.

Readily Received in America
To date, most cognitive enhancement research has been done in Europe because the FDA is opposed to garden-variety usage of drugs, nutrients, and - believe it or not! - even foods.2 Nevertheless, the desire to be smarter and use one's brain more ably is a powerful motive for human action. It didn't matter that vinpocetine was late to arrive on American shores. The knowledge that it is the first full-fledged nootropic (a supplement positively affecting the mind) has stirred considerable excitement. Jumping on the subject, The Wall Street Journal, ever alert to enhanced-productivity news, covered vinpocetine in its weekly health column, but did so inadequately, with a reviewer quite conventional in her convictions and bound by a belief system loosely describable as "father knows best."3

Researchers found vinpocetine to be safe and non-toxic with an amazing array of functional and structural benefits for improved health. 

Poor Reviews Fuel Good Ones
Despite all efforts to date to play down its value, when the public truly becomes aware of the versatility of vinpocetine as promoter of mind as well as body, good reviews will come - just as they have slipped through into the popular press a few times in the past. Once the Geni of good ideas is released, it is unstoppable. As American researcher Victor DeNoble told The Chemical Marketing Reporter one decade after the European awakening to its virtues, "Vinpocetine appears to improve a person's ability to acquire new memories and to restore memories that have been disrupted."4 What a grand accolade! Vinpocetine is as exciting as nootropic nutrients get.

"Smart Drug" aficionado Ward Dean, MD has commended vinpocetine. "It's one of the few cognitive enhancers that I actually notice [a positive difference] when I take it."5 One of vinpocetine's mechanisms actually protects against excitotoxic excesses,6 so in a sense, vinpocetine allows you to have your cake and eat it too. Figuratively, vinpocetine comes with the struts, shocks, and suspension system of an expensive (and exciting) German sports car.

Vinpocetine is Like Viagra® for the Brain
The earliest investigations of vinpocetine resulted in its utilization for the treatment of cerebrovascular dysfunctions. Since then it has become a reference compound in the pharmacological research of cognitive deficits caused by hypoxia (not getting enough oxygen) and ischemia (not getting enough blood, which carries oxygen and glucose). Experimental data indicates that vinpocetine provides a considerable neuroprotective effect.

The Wall Street Journal, ever alert to enhanced-productivity news, covered vinpocetine in its weekly health column. 

Through its inhibition of a key enzyme, phosphodiesterase type 1 (PDE1), vinpocetine increases vascular smooth muscle function in much the same way that Viagra works, albeit in a different area of the body. Viagra inhibits phosphodiesterase type 5 (PDE5), which like vinpocetine, increases amounts of the nucleotide cyclic GMP, a so-called second messenger, directly responsible for the muscle-relaxing effects. In the penis, the result is a widening of the vascular openings allowing blood to fill the penis. In the brain, blood flows more effortlessly. In a sense, vinpocetine is Viagra for the brain. Its ability to reduce resistance in cerebral vessels and increase cerebral flow contributes favorably to its neuroprotective effect.

From the Beginning
Following the earliest studies, the quality of international scientific literature supporting vinpocetine's cerebral blood flow enhancement abilities7-9 and its direct relaxing effect on the smooth muscle of cerebral arteries have burgeoned.10-12 Data showing its anti-hypoxic,13,14 anti-ischemic15-18 and anti-convulsant effects19,20 have also proven fertile, resulting in a better understanding of vinpocetine's mechanisms. Inhibition of PDE1, in addition to increasing cGMP, also increases cAMP in cerebral arteries and microvessels and further potentiates the ability of noradrenaline to increase cAMP buildup.21,22 At the same time, clinical trials have confirmed that vinpocetine inhibits platelet aggregation and enhances the deformability of red blood cells too.23,24 Platelet aggregation increases the likelihood of blood clots and severe blood (and therefore oxygen and glucose) disruption to the brain. Deformability is a desireable characteristic of blood that gives it structural flexibility and allows it to remain useful under stressful conditions.

"Vinpocetine appears to improve a person's ability to acquire new memories and to restore memories that have been disrupted." 

At least 700 articles have been published over the last 25 years on vinpocetine including chemical, analytical, pharmaceutical, technological and clinical reports. More than 200 research studies have been done on both animals and humans. Yet no overall understanding of the way vinpocetine works has been articulated until recently. Each of the subsections that follows represents a significant piece of the answer.

Red Blood Cell Deformability is a Good Thing
To protect your brain against thrombosis, it is useful to maintain high deformability of red blood cells and to prevent excessive platelet aggregation. The flip side is to enhance blood flow conditions by decreasing the viscosity of blood and rigidity of red blood cells.

Essentially, this enhances blood circulation and perfusion of tissues. Also of high importance is the prevention of cerebral ischemia (reduction of blood availability) as well as improvement of  circulation even in areas of the brain where shortage of blood already exists.

In a sense, vinpocetine is Viagra® for the brain. 

When vinpocetine was given orally to healthy volunteers, deformability of red blood cells improved significantly.25 The same researcher also showed that 30 mg of vinpocetine per day could achieve similarly significant deformability improvements in stroke patients.26 Other studies have shown vinpocetine to have benefits in a combined total of 163 humans for decreased intravascular coagulation, inhibited platelet aggregation,27 and reduced blood viscosity.28 A study by Tohgi29 found that vinpocetine increased the ATP levels in red blood cells which, in turn, resulted in better stimulation, release, and absorption of oxygen by hemoglobin in vascular dementia patients.

Pro-Memory and Anti-Amnesia
One of the most extraordinary benefits of vinpocetine is its ability to enhance memory function. Given that loss of memory is more of an obvious problem when the brain has sustained oxygen damage, early studies focused on patients with this pathological condition. At first, mice studies30,31 found vinpocetine to be proactive in relieving anoxia (total oxygen loss) while other studies showed that it has a protective influence even when sustaining total loss of blood circulation.32,33 Yet other studies have shown it to prevent cell toxicity caused by the cut-off of oxygen34 and to protect both mice and rats form carotid occlusion.35,36

To protect your brain against thrombosis, it is useful to maintain high deformability of red blood cells and to prevent excessive platelet aggregation.

When vinpocetine was given to rats along with amnesia-producing drugs, DeNoble37 demonstrated improved memory. Vinpocetine offered protection against cognitive damages in amnesia-induced mice and rats.38,39

Experiments have also been carried out concerning the neuroprotective effects of vinpocetine. Various studies have shown that it can recover 25% of areas of the brain considered to be necrosed (dead);40,41 it can inhibit 50% of drug-induced neuronal loss;42-44 and it can help maintain long-term efficiency of glucose utilization.

Jucker45 noted changes in patterns of attention and mobility as well as reductions in the glucose uptake of several brain structures in older animals, compared to the control group of younger animals. Vinpocetine administration for six weeks led to improvements of behavioral performances and stimulated glucose uptake in the brain, without an increase in glucose utilization.

One of the most extraordinary benefits of vinpocetine is its ability to enhance memory function.

Regaining Memory
Vinpocetine in dosages of 1-10 mg per kg of weight improved learning and memory processes and protected against dementia caused by ischemia or hypoxia.46,47 There were no significant side effects in the central nervous system.48 At doses of 0.5-3 mg per kg of body weight, vinpocetine improved the learning process of young animals impaired by classic memory-blocking drugs.49

Long-Term Memory
Perhaps no feature of memory is more desired than long-term memory. People constantly complain, especially with age, that new data seems to crowd out the old, or that things committed to memory are not very accessible after an extended period of time. In technical terms, this aspect of memory is referred to as long-term potentiation (LTP) and it results from the long-term enhancement of synaptic efficiency or neuronal plasticity.

Vinpocetine inhibits platelet aggregation and enhances the deformability of red blood cells too.

Thus, LTP is the standard by which compounds are often researched when looking for cognitive process enhancement. It is "the elephant never forgets" model of memory.

LTP findings with vinpocetine were first reported by Japanese researchers50 who reported that low concentrations of vinpocetine could cause an important microelectrophysiological measurement of LTP to triple. While these results were supported by in vitro models (not in the body), another study soon followed51 with the same pattern-type showing in cats: vinpocetine dosage of 5 mg per kg significantly potentiated LTP. When this study was followed up, vinpocetine administered orally (5 mg per kg for 6 days) completely restored the reduced LTP.52 From these studies it was possible to say that the data unambiguously supports the fact that vinpocetine is capable both in vitro and in vivo of improving LTP, i.e. the synaptic plasticity which is regarded to be the cellular model of learning.

Other microelectrophysiological studies show that when vinpocetine is given orally to anaesthetized animals, the noradrenergic activity emanating outward from the locus coeruleus is enhanced.53 The locus coeruleus is a part of the brain at the base of the neck, behind the cerebellum. Noradrenergic cell loss in the locus coeruleus in Alzheimer's disease is related to cognitive decline.54 This phenomenon is true also for the classical nootropic drugs piracetam or hydergine which reduce cognitive damages.55 Thus we may surmise that vinpocetine is capable of enhancing cognitive functions too.

Vinpocetine offered protection against cognitive damages in amnesia-induced mice and rats. 

Protecting Your Neurons
The neuroprotective effects of vinpocetine are well established. When the effects of antioxidants on glutamate-damaged tissue were studied, vinpocetine was able to completely abolish neuronal injury.56 Although not usually thought of as an antioxidant, vinpocetine is quite competent. According to recent research,57-59 vinpocetine effectively protects against drug-induced cell loss in primer cortical tissue culture, a feat that is approximately 100 times more effective than Dilantin®. Dilantin is a well-received drug among longevists, but with clear side effects, especially when taken at higher levels. Side effects may include hyperactivity, behavioral problems, sedation, and even dementia.

Another scientific paper found that vinpocetine has a neuroprotective effect owing to its ability to inhibit adenosine uptake,60 but that it also has neuroprotective effects independent of this.61 Relatively large amounts of caffeine can inhibit adenosine, thereby producing a stimulating effect.62 Vinpocetine is known to provide a clear but mild stimulation for some users.

Some new data indicates that vinpocetine has a gastroprotective effect, decreases inflammatory reactions and has antiarthritic qualities. 

Other Effects of Vinpocetine
Some new data indicates that vinpocetine has a gastroprotective effect,63 decreases inflammatory reactions and has antiarthritic qualities too.64 The compound also inhibited the formation of arteriosclerotic plaques.65,66

How Does Vinpocetine Work?
Vinpocetine's influence as a dietary supplement is thought to occur principally because of its ability to restore function associated primarily with age-related declines of blood flow, oxygen utility, and cellular function(s). The latest thinking is that there are several effects involved simultaneously in the mechanism of action of  vinpocetine, although each relatively depends on a number of factors, including but not limited to . . .

  1. The organic system affected (including cell population)
  2. The functions and their physiological condition (compared with a healthy young adult)

Another scientific paper found that vinpocetine has a neuroprotective effect owing to its ability to inhibit adenosine uptake. 

Highlights of the mechanism of action of vinpocetine include:

1) The Phosphodiesterase-Inhibitory Effect
Already described above and similar to the Viagra effect, when vinpocetine inhibits the isoenzyme phosphodiesterase (type I), it increases the level and activity of the cyclic nucleotide GMP. Thus, the compound may increase cGMP and its response ability, resulting in a vascular effect for the improvement of cerebral circulation as well as for the effect exerted on platelets. However, it is not yet clear how this mechanism is related to vinpocetine's cerebro- and neuro-protective effects.

2) Effects Exerted on Ion-Channels
Vinpocetine exercises an electrophysical influence by directly blocking the sodium channel (Na+) operation at the neuronal level. This in turn regulates calcium channel operations (Ca2+) preventing abnormally high intracellular Ca2+ concentrations following oxygen or blood flow disruptions (hypoxia or ischemia) or both. This inhibition (of Na+ channels), and reduction (of intracellular Ca2+ levels) is thought to moderate the excitotoxicity of neurotransmitters such as glutamate, which are released due to the effect of ischemia or hypoxia. Vinpocetine may thus prevent the initiation of intracellular molecular cascades that may result in the irreversible damaging of neurons. In this way, vinpocetine produces neuro- and cerebro-protective effects.

3) Uptake-Inhibitory Action
Vinpocetine inhibits adenosine uptake. Adenosine is an inhibiting neurotransmitter. Thus, especially in hypoxia and ischemia (when the large-scale declines of ATP can lead to the increase in extracellular adenosine concentration), adenosine reduces Ca2+ channel activity which can result in excitotoxic damage. At the same time, it can inhibit excessive release of glutamate which can have an excitotoxic effect [see Figure 1].

Figure 1: Presumable mechanisms of action of vinopocetine.

Vinpocetine blocks the sodium channel (Na+) operation at the neuronal level, which regulates calcium channel (Ca2+) operations preventing high intracellular Ca2+ concentrations. Lessening neurotransmitter excitotoxicity may result, lowering ischemic or hypoxic damage and providing cerebro-protective effects. Vinpocetine also inhibits uptake of the neurotransmitter adenosine. This reduces Ca2+ channel activity preventing excitotoxic damage. Also shown is vinpocetine's inhibition of the enzyme phosphodiesterase type I (PDE1) lessening cGMP and relaxing blood vessel muscles and increasing cAMP.  PDE1 is dependant on calmodulin (CaM), a calcium binding protein, which is weakly inhibited by vinpocetine. CaM is weakly inhibited by Ca2+. Vinpocetine may weakly inhibit the effect of CaM on PDE1 either through inhibition of calmodulin or its effect on Ca2+. CaM increases nitric oxide's relaxation effect by increasing cGMP.


  1. Riddle J. Dioscorides on Pharmacy and Medicine. Austin: University of Texas Press, 1985.
  2. The FDA holds to its paternalistic view out of what they construe to be their self interest. They are, first of all, bureaucrats and regulators whose livelihood is threatened by anything that helps make people more responsible, and less in the debt of the experts who make decisions for them. Think of them as bad wizards.
  3. Chase M. New supplement aims to boost memory but proof is scanty. The Wall Street Journal. July 13, 1998;pp. B1.
  4. Anon. Chemical Marketing Reporter 1986;229:7.
  5. Dean W. Q&A: Vincamine? Smart Life News. 1998;6(4):12.
  6. Erdo SL, Nin-sheng C, Wolff JR, Kiss B. Vinpocetin protects against excitotoxic cell death in primary cultures of rat cerebral cortex. Eur J Pharmacol. 1990;187(3):551-553.
  7. Imamoto T, Tanabe M, Shimamoto N, Hirata M. Effects of vinpocetine and its metabolite apo vincaminic-acid on cerebral and peripheral circulation in anesthetized dogs Jpn J Pharmacol 1983;33(Suppl):296.
  8. Imamoto T, Tanabe M, Shimamoto N, Kawazoe K, Hirata M. Cerebral circulatory and cardiac effects of vinpocetine and its metabolite, apovincaminic acid, in anesthetized dogs. Arzneimittelforschung 1984;34(2):161-169.
  9. Sugawa M, Tanabe S, Ikeda Y, Noda Y. Effects of dibenzoxazepines on regional cerebral blood flow in conscious cats. Jpn J Pharmacol. 1986;40(Suppl):119.
  10. Mchedlishvili GI, Ormotsadze LG. The effect of ethyl apovincaminate on vasospasm of the circulatory isolated internal carotid artery in dogs. Arzneim-Forsch. 1981;31(3):414-418.
  11. Plotnikov MB, Kotov AN. Mechanism of the vasodilator action of kavinton on the cerebral vessels. Farmakol Toksikol. 1983;46:36.
  12. Gabrielyan ES, Akopov SE, Balayan BG. Prostacyclin effect on cerebral vessels and its pharmacological modulation 1986 Byul Eksp Biol Med. 1986;102:717-719.
  13. Kiss B, Lapis E, Pálosi E, Groó D, Szporny L. Protection of tissues against hypoxia, Elsevier Biomedical Press, Amsterdam 1982:p3 OS-3 09.
  14. Nikolova M, Nikolov R, Milanova D. Anti-hypoxic effect of piracetam and interaction with prostacyclin. Meth Find Exp Clin Pharmacol. 1984;6:367.
  15. Kakihana M, Sun M, Shibota M, Hamajo K, Nagaoka A. Protective effect of vinpocetine on experimental brain ischemia. Folia Pharmacol Japon. 1982;80:225.
  16. Milanova D, Nikolov R, Nikolova M. Study on the anti-hypoxic effect of some drugs used in the pharmacotherapy of cerebrovascular disease. Meth Find Exp Clin Pharmacol. 1983;5(9):607-612.
  17. King GA, Narcavage D, Romanski L, Hanig D, Shieh A. Effects of vinpocetine in a rat model of cerebral ischemia. Neurosci Abstr. 1985;11:433.
  18. King GA, Narcavage D. Comparison of the effects of vinpocetine, vincamine, phenytoin, and cinnarizine in a rat model of cerebral ischemia. Drug Dev Res. 1986;9:225-231.
  19. Dutov AA, Tolpyshev BA, Karpov VN, Petrov AP. Pharmacological analysis of the anticonvulsant action of kavinton. Farmakol Toksikol. 1987;50:17-20.
  20. Dutov AA, Tolpyshev BA, Karpov VN, Petrov AP. Effect of Cavinton on convulsions caused by chemical substances. Farmakol Toksikol. Jul-Aug 1986;49(4):22-5.
  21. Lapis E, Kiss B, Szporny L. Advances in Cyclic Nucleotide and Protein Phosphorylation Research 1983;17A:138.
  22. Lapis E, Kiss B, Szporny L. The effect of chronic vinpocetine treatment on the cyclic amp accumulation in guinea-pig cerebral arteries and microvessels in-vitro. Acta Physiol Hung. 1984; 63(3-4):351.
  23. Kuzuya F. Effects of vinpocetine on platelet aggregability and erythrocyte deformability. Ther Hung. 1985;33:22-34.
  24. Osawa M, Maruyama S. Effects of TCV-3B (vinpocetine) on blood viscosity in ischemic cerebrovascular diseases. Ther Hung 1985; 33(1):7-12.
  25. Hayakawa M. Effect of vinpocetine on red blood cell deformability in vivo measured by a new centrifugation method. Arzneim-Forsch. 1992;42(3):281-283.
  26. Hayakawa M. Effect of vinpocetine on red blood cell deformability in vivo measured by a new centrifugation method. 1992;42(3):281-283. Arzneim-Forsch. 1992;42(4):425-427.
  27. Lebedeva NV, Lobkova TN, Ionova VG, Kharapova EV. Klin Med. 1990; 68, 31.
  28. Szobor A, Klein M. Examinations of the relative fluidity in cerebrovascular disease patients. Ther Hung. 1992;40:8-11.
  29. Tohgi H , Sasaki K, Chiba K, Nozaki Y. Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type. Arzneim-Forsch. 1990;40:640-643.
  30. King GA. Protective effects of vinpocetine and structurally related drugs on the lethal consequences of hypoxia in mice. Arch Int Pharmacodyn Ther. 1987;286, 299-307.
  31. Yamamoto M, Shimizu M, Kawabata S. Cerebral vasodilators potentiate the anti-anoxic activity of indeloxazine hydrochloride a new cerebral activator. Neuropharmacology 1989;28:313-317.
  32. Yamada S, Yamaguchi K, Okuyama S. Cerebral protective effects of VA-045, a novel apovincaminic acid derivative, in mice. Res Commun Mol Pathol Pharmacol 1994 Oct;86(1):83-91.
  33. Ibid.
  34. Lamar J-C, Poignet H, Beughard M, Dureng G. Calcium antagonist activity of vinpocetine and vincamine in several models of cerebral ischemia. Drug Dev Res. 1988;14:297-304.
  35. Takeo S, T anonaka K, Hirano T, Miyake K, Okamoto J. Cerebroprotective action of naftidrofuryl oxalate I: Prolongation of survival time and protection of cerebral energy metabolism in bilateral carotid artery-ligated mice. Folia Phannacol Japon. 1988;91:267-273.
  36. Vaizov VK, Plotnikova TM, Yakimova TV, Vaizova OE, Saratikov AS. Ammonium succinate - an effective corrector of cerebral circulatory hypoxia. Biull Eksp Biol Med 1994 Sep;118(9):276-278.
  37. DeNoble VJ, Repetti SJ, Gelpke LW, Wood LM, Keim KL. Vinpocetine: nootropic effects on scopolamine-induced and hypoxia-induced retrieval deficits of a step-through passive avoidance response in rats. Pharmacol Biochem Behav. 1986;24:1123.
  38. Groó D, Pálosi É, Sporny L. Comparison of the effect of vinpocetine vincamine and nicergoline on the normal and hypoxia-damaged learning process in spontaneously hypertensive rats. Drug Dev Res. 1988;15:75-86.
  39. Groó D. Pálosi É, Sporny L. Cognitive enhancers prevent the hypoxia-induced disruption of conditioned avoidance response. Drug Dev Res. 1989;18:19-28.
  40. Backhaus C, Karkouthly C, Welsch M, Krieglstein J. J Pharmacol Toxicol Methods. 1992; 27, 27.
  41. Bielenberg Gw. Effects of vincamine and vinpocetine on infarct size in focal cerebral ischemia. Arch Pharmacol. 1992;345(Suppl):R122.
  42. Rischke R, Krieglstein J. Increased LCGU and decreased LCBF in rat hippocampus 7 days after ischemia. J Neurochem. 1989;52(Suppl):S56.
  43. Rischke R, Krieglstein J. Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat. Pharmacology 1990; 41:153-160.
  44. Rischke R, Krieglstein J. Protective effect of vinpocetine against brain damage caused by ischemia. Jpn Pharmacol. 1991; 56:349-356.
  45. Jucker M, Meier-Ruge W, Baettig K. Pychopharmacology (Berlin) 1988;96:29.
  46. Pálosi E, Szporny L. Effects of ethyl apovincaminate on the central nervous system Arzneim-Forsch. 1976;26:1926-1929.
  47. Keim KL, Hall PC. General neuropharmacology of vinpocetine: A putative cerebral activator. Drug Dev Res. 1987;11:107-115.
  48. Ibid.
  49. Paroczai M, Kiss B, Karpati E.Effect of RGH-2716 on learning and memory deficits of young and aged rats in water-labyrinth. Brain Res Bull 1998 Mar 15;45(5):475-488.
  50. Ishihara K, Katsuki H, Sugimura M, Satoh M. Idebenone and vinpocetine augment long-term potentiation in hippocampal slices in the guinea-pig. Neuropharmacology 1989; 29:569-574.
  51. Molnár P, Gaál L. Eur. Effect of different subtypes of cognition enhancers on long-term potentiation in the rat dentate gyrus in vivo. J Pharmacol. 1992; 215:17-22.
  52. Molnár P, Gaál L, Horvát C. The impairment of long-term potentiation in rats with medial septal lesion and its restoration by cognition enhancers. Neurobiology 1994;2:255-266.
  53. Gaál L, Molnár P. Effect of vinpocetine on noradrenergic neurons in rat locus coeruleus. Eur J Pharmacol. 1990;187:537-539.
  54. Hoogendijk WJ, Feenstra MG, Botterblom MH, Gilhuis J, Sommer IE, Kamphorst W, Eikelenboom P, Swaab DF. Increased activity of surviving locus ceruleus neurons in Alzheimer's disease. Ann Neurol 1999 Jan;45(1):82-91.
  55. Olpe H-R, Steinmann MW, Jones RS. Locus coeruleus as a target for psychogeriatric agents. Ann NY Acad Sci. 1985;444:395-405.
  56. Miyamoto M, Murphy TM, Schnaar RL, Coule JT. Antioxidants protect against glutamate-induced cytotoxicity in a neuronal cell line. J Pharm Exp Ther. 1989; 250:1132-1140.
  57. Lakics V, Molnár P, Bencze JZ, Erdö SL. J Neurochem. 1995a;65:158.
  58. Lakics V, Sebesryén MG, Erdo SL. Vinpocetine is a highly potent neuroprotectant against veratridine-induced cell death in primary cultures of rat cerebral cortex. Neurosci Lett. 1995b;185:127-130.
  59. Erdö SL, Molnár P, Lakics V, Bence JZ, Tömösközi Z. Vincamine and vincanol are potent blockers of voltage-gated Na+channels. Eur J Pharmacol. 1996;314(1-2 ):69-73.
  60. Krieglstein J, Rischke R. Eur. Vinpocetine increases the neuroprotective effect of adenosine in-vitro. J Pharmacol. 1991;205:7-10.
  61. Milusheva E, Sperlágh B, Kiss B, Szporny L, Pásztor E, Papasova M, Vezi ES. Inhibitory effect of hypoxic condition on acetylcholine release is partly due to the effect of adenosine released from the tissue. Brain Res Bull. 1990;24:369.
  62. Nehlig A, Daval JL, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Rev 1992 May-Aug;17(2):139-70.
  63. Nosálová V, Machová J, Babulová A. Protective action of vinpocetine against experimentally induced gastric damage in rats. Arzneim-Forsch. 1993; 43:981-985.
  64. Prokopová A, Revensky J, Machová J, Stanciková M, Orvisky E, Kéry, V. Effect of vinpocetine on rat adjuvant arthritis. Int J Immunopathol Pharmacol. 1992;5:193-199.
  65. Yasui M, Yano I, Ota K, Oshima A. Preventive effect of vinpocetine on calcifications atherosclerosis in experimental rabbits. Acta Neurol Scan. 1989;79:239-242.
  66. Yasui M, Yano I, Ota K, Oshima AJ. Calcium phosphorus and aluminum concentrations in the central nervous system, liver and kidney of rabbits with experimental atherosclerosis preventive effects of vinpocetine on the deposition of these elements. Internat Med Res. 1990;18:142-152.

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