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On the possible role of central monoaminergic systems in the central nervous system actions of vinpocetine
Author(s) -
Kiss Béla,
Szporny László
Publication year - 1988
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430140318
Subject(s) - monoaminergic , vinpocetine , monoamine neurotransmitter , dopamine , chemistry , medicine , endocrinology , serotonin , central nervous system , catecholamine , pargyline , neurotransmitter , pharmacology , biology , biochemistry , receptor
The effects of vinpocetine, a recently described cerebral blood flow enhancer having antihypoxic, anti‐ischemic, and cognitive‐function‐improving actions, on rat brain monoaminergic neurotransmission have been studied under normoxic and hypoxic conditions. Vinpocetine slightly affected the steady‐state levels of monoamines and their metabolites in whole brain, but a tendency was seen to increase dopamine (DA) and its metabolites in lower brain parts and to reduce noradrenaline (NA) in “terminal” regions. MHPG‐SO 4 levels were enhanced in whole brain and in almost all regions examined. There was a tendency to increase 5‐hydroxyindole‐acetic acid (5‐HIAA) in some areas. It accelerated the whole brain NA turnover dose‐dependenntly, but left that of DA unchanaged. Enhancement of NA turnover was most noted in the lower brain areas. On the other hand, no change was found in DA accumulation, an index of heart NA turnover after inhibition of dopamine‐beta‐hydroxylase. The rate of probenecideinduced accumulation of cerebral MHPG‐SO 4 and, to a lesser extent, that of 5‐HIAA was also increased. No change was seen in the pargyline‐induced serotonin (5‐HT) accumulation. Although vinpocetine had slight or no effects on regional levels of monoamines and their metabolites, and did not alter their in vivo biosynthesis rate under normoxic conditions, it was able partially or totally to prevent reductions in the biosynthesis rate of monoamines and antagonized the decrease of NA, 5‐HT, and 5‐HIAA (but not that of DA) induced by normobaric hypoxia. This effect was mainly confined to lower brain areas. From the results, we conclude that vinpocetine primarily affects cell body regions (e.g., brainstem) of the rat brain. Enhancement of the activity of ascending noradrengergic and, perhaps, serotoninergic pathways may very likely participate in the cognitive function‐imporving actions of the drug under normoxic conditions. Vinpocetine was able to prevent monoamigergic neurotransmission against deleterious effects of hypoxia.