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Titolo:
MECHANISMS OF AMPHETAMINE ACTION REVEALED IN MICE LACKING THE DOPAMINE TRANSPORTER
Autore:
JONES SR; GAINETDINOV RR; WIGHTMAN RM; CARON MG;
Indirizzi:
DUKE UNIV,MED CTR,HOWARD HUGHES MED INST LABS,DEPT CELL BIOL,BOX 3287DURHAM NC 27710 DUKE UNIV,MED CTR,HOWARD HUGHES MED INST LABS,DEPT CELL BIOL DURHAM NC 27710 DUKE UNIV,MED CTR,HOWARD HUGHES MED INST LABS,DEPT MED DURHAM NC 27710 UNIV N CAROLINA,DEPT CHEM CHAPEL HILL NC 27599 UNIV N CAROLINA,CURRICULUM NEUROBIOL CHAPEL HILL NC 27599
Titolo Testata:
The Journal of neuroscience
fascicolo: 6, volume: 18, anno: 1998,
pagine: 1979 - 1986
SICI:
0270-6474(1998)18:6<1979:MOAARI>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
VESICULAR MONOAMINE TRANSPORTER; RAT-BRAIN SYNAPTOSOMES; SYNAPTIC VESICLES; NUCLEUS-ACCUMBENS; CAUDATE-PUTAMEN; ACETYLCHOLINE NEUROTRANSMISSION; MOLECULAR MECHANISMS; SYNTHESIS INHIBITORS; TRANSMITTER STORES; AMINE TRANSPORTERS;
Keywords:
AMPHETAMINE; DOPAMINE TRANSPORTER; KNOCKOUT; MICE; VOLTAMMETRY; RO4-1284; TETRABENAZINE; SYNAPTIC VESICLES; MICRODIALYSIS; DOPAMINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
S.R. Jones et al., "MECHANISMS OF AMPHETAMINE ACTION REVEALED IN MICE LACKING THE DOPAMINE TRANSPORTER", The Journal of neuroscience, 18(6), 1998, pp. 1979-1986

Abstract

Amphetamine (AMPH) inhibits uptake and causes release of dopamine (DA) from presynaptic terminals. AMPH can act on both vesicular storage of DA and directly on the dopamine transporter (DAT). To assess the relative importance of these two processes, we have examined the releasing actions of AMPH in mice with a genetic deletion of the DAT. The sequence of actions of AMPH has been determined by following the real timechanges of DA in the extracellular fluid of intact tissue with fast scan cyclic voltammetry. In striatal slices from wild-type mice, AMPH causes a gradual (similar to 30 min) increase in extracellular DA, witha concomitant disappearance of the pool of DA available for depolarization-evoked release. Conversely, in slices from mice lacking the DAT,although a similar disappearance of electrically stimulated DA release occurs, extracellular DA does not increase. Similarly, microdialysismeasurements of DA after AMPH in freely moving animals show no changein mice lacking the DAT, whereas it increases 10-fold in wild-type mice. In contrast, redistribution of DA from vesicles to the cytoplasm by the use of a reserpine-like compound, Ro4-1284, does not increase extracellular DA in slices from wild-type animals; however, subsequent addition of AMPH induces rapid (<5 min) release of DA. Thus, the DAT isrequired for the releasing action, but not the vesicle-depleting action, of AMPH on DA neurons, and the latter represents the rate-limitingstep in the effects of AMPH. Furthermore, these findings suggest thatin the absence of pharmacological manipulation, such as the use of amphetamine, endogenous cytoplasmic DA normally does not reach sufficient concentrations to reverse the DAT.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 15:35:17