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Titolo:
Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings
Autore:
Trejo, F; Nekrassov, V; Sitges, M;
Indirizzi:
Natl Autonomous Univ Mexico, Inst Invest Biomed, Mexico City 04510, DF, Mexico Natl Autonomous Univ Mexico Mexico City DF Mexico 04510 04510, DF, Mexico Inst Nacl Comunicac Humana, SSA, Mexico City, DF, Mexico Inst Nacl Comunicac Humana Mexico City DF Mexico Mexico City, DF, Mexico
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 909, anno: 2001,
pagine: 59 - 67
SICI:
0006-8993(20010803)909:1-2<59:COVEOD>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE CEREBRAL-ISCHEMIA; DOPAMINE RELEASE; CHROMAFFIN GRANULE; ACTIVE-TRANSPORT; NEURONAL DEATH; IN-VITRO; H-3 GABA; RAT; TERMINALS; SYNAPTOSOMES;
Keywords:
neuroprotection; MAO-A; ischemia; synaptic vesicle; Na+ channel; striatal synaptosome;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Sitges, M Natl Autonomous Univ Mexico, Inst Invest Biomed, Apartado Postal70228, Mexico City 04510, DF, Mexico Natl Autonomous Univ Mexico Apartado Postal 70228 Mexico City DF Mexico 04510
Citazione:
F. Trejo et al., "Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings", BRAIN RES, 909(1-2), 2001, pp. 59-67

Abstract

The effect of vinpocetine, a nootropic drug with anti-ischemic potential, on the release of DA and its main metabolite, DOPAC, was investigated in striatum isolated nerve endings under resting and depolarized conditions. Vinpocetine does not modify the baseline release of DA or the exocytotic release of DA evoked by high K+, but inhibits the release of DA evoked by veratridine reversal of the DA transporter. In addition to these results, which confirm the vinpocetine selective blockade of voltage-sensitive presynaptic Na channels (VSSC) previously reported [Neurochem. Res. 24 (1999) 1585], vinpocetine increases DOPAC release either under resting, veratridine or highK+ depolarized conditions. This latter effect, which does not involve VSSC, was characterized. The parallel determination of the released and retained catecholamine concentrations revealed that vinpocetine increases DOPAC release at the expense of internal DA in a dose-dependent manner (low LM range). In contrast to vinpocetine, the selective MAO-A inhibitor, clorgyline, increases DA and decreases DOPAC formation. The combined action of vinpocetine and clorgyline does not indicate, however, that the activation of MAO is the mechanism responsible for the increase in DOPAC caused by vinpocetine. Reserpine, although more potent and efficient than vinpocetine, qualitatively exerts the same pattern of changes on DA and DOPAC concentrations. It is concluded that, in addition to the inhibition of presynaptic VSSC permeability, which selectively inhibits the transporter-mediated release of all neurotransmitters, vinpocetine increases DOPAC by impairing the vesicular storage of DA. Our results indicate that the cytoplasm extravesicular DA is metabolized by MAO to DOPAC. Most of the DOPAC formed is exported to the extracellular medium. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 03:21:26