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Titolo:
Gamma vinyl-GABA differentially modulates NMDA antagonist-induced increases in mesocortical versus mesolimbic DA transmission
Autore:
Schiffer, WK; Gerasimov, M; Hofmann, L; Marsteller, D; Ashby, CR; Brodie, JD; Alexoff, DL; Dewey, SL;
Indirizzi:
Brookhaven Natl Lab, Dept Chem, Upton, NY 11973 USA Brookhaven Natl Lab Upton NY USA 11973 ab, Dept Chem, Upton, NY 11973 USA NYU, Sch Med, Dept Psychiat, New York, NY USA NYU New York NY USANYU, Sch Med, Dept Psychiat, New York, NY USA
Titolo Testata:
NEUROPSYCHOPHARMACOLOGY
fascicolo: 5, volume: 25, anno: 2001,
pagine: 704 - 712
SICI:
0893-133X(200111)25:5<704:GVDMNA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
VENTRAL TEGMENTAL AREA; MEDIAL PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS DOPAMINE; DUAL-PROBE MICRODIALYSIS; PHENCYCLIDINE-INDUCED HYPERACTIVITY; AMINO-ACID RECEPTORS; FREELY MOVING RATS; AMINOBUTYRIC-ACID; GLUTAMATERGIC REGULATION; SUBSTANCE-ABUSE;
Keywords:
phencyclidine; NMDA-antagonist; microdialysis; dopamine; glutamate; GABA; vigabatrin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Schiffer, WK Brookhaven Natl Lab, Dept Chem, Upton, NY 11973 USA Brookhaven Natl Lab Upton NY USA 11973 , Upton, NY 11973 USA
Citazione:
W.K. Schiffer et al., "Gamma vinyl-GABA differentially modulates NMDA antagonist-induced increases in mesocortical versus mesolimbic DA transmission", NEUROPSYCH, 25(5), 2001, pp. 704-712

Abstract

To explore the role of endogenous GABA in NMDA antagonist induced dopamine(DA) release, we used in vivo microdialysis to study the effects of pretreatment with gamma -vinyl GABA (GVG) on phencyclidine (PCP)-induced DA release in terminal regions of midbrain DA neurons. GVG, an irreversible inhibitor of the GABA catabolizing enzyme GABA-AT, significantly reduced the DA response to PCP (TO mg/kg) in freely moving animals. Preferential increases in PCP-induced DA release in the PFC (four-fold those of NAcc) were dose-dependently inhibited by acute pretreatment with GVG at doses of 150 (51% inhibition), 300 (68% inhibition), and 500 (82% inhibition) mg/kg, whereas NAccPCP-induced DA activity was unresponsive to 150 mg/kg and only partially inhibited by 300 and 500 mg/kg. Subchronic treatment with GVG did not enhance the inhibitory capacity of the GABAergic system. While GVG evidently modulates PCP-induced increases in mesocorticolimbic DA transmission, the character of this modulation is regionally specific, with cortical NMDA-antagonist induced increases appearing more sensitive to inhibition by endogenous GABA than subcortical areas. (C) 2001 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.

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Documento generato il 18/01/20 alle ore 10:43:29