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Titolo:
METHAMPHETAMINE-INDUCED ALTERATIONS IN DOPAMINE TRANSPORTER FUNCTION
Autore:
BENNETT BA; HOLLINGSWORTH CK; MARTIN RS; HARP JJ;
Indirizzi:
WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PHYSIOL & PHARMACOL,MED CTRBLVD WINSTON SALEM NC 27157
Titolo Testata:
Brain research
fascicolo: 1-2, volume: 782, anno: 1998,
pagine: 219 - 227
SICI:
0006-8993(1998)782:1-2<219:MAIDTF>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE-HYDROXYLASE ACTIVITY; FETAL RAPHE NEURONS; STRIATAL DOPAMINE; BEHAVIORAL SENSITIZATION; NUCLEUS-ACCUMBENS; H-3 DOPAMINE; RAT STRIATUM; CATECHOLAMINE UPTAKE; CORPUS STRIATUM; BIOGENIC-AMINES;
Keywords:
DOPAMINE; METHAMPHETAMINE; TRANSPORTER; RELEASE; MIDBRAIN CULTURE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
B.A. Bennett et al., "METHAMPHETAMINE-INDUCED ALTERATIONS IN DOPAMINE TRANSPORTER FUNCTION", Brain research, 782(1-2), 1998, pp. 219-227

Abstract

Repeated methamphetamine (METH) administration has been shown to produce differing neurochemical as well as behavioral effects in rats. This study was designed to examine the effects of acute and chronic METH exposure on uptake and release of [H-3]dopamine (DA) in cultured midbrain dopamine neurons to determine if persistent neuronal adaptations ensue. In addition, we have assessed DA D2 receptor function to determine if chronic METH alters this receptor. Fetal midbrain cultures were exposed to METH (1, 10 mu M) for 5 days and dopaminergic function examined 1 or 7 days after drug removal. The ability of METH to release [H-3]DA was compared to other releasing agents as well as several potentuptake inhibitors. Chronic exposure to a release-promoting concentration of METH resulted in either no change or a reduction in [H-3]DA release upon subsequent METH challenge. Pretreatment with METH was also found to cause a decrease in the B-max for [H-3]raclopride binding, suggesting that persistently elevated DA levels cause a downregulation ofDA D2 receptors. Examination of transporter kinetics utilizing initial velocity of uptake revealed that METH treatment caused a significantdecrease in affinity (K-m) for the substrate (DA), while not alteringthe maximal velocity of uptake (V-max). Binding studies with [I-125]RTI-55 revealed that there was no alteration in either the B-max or K-dfor this ligand, suggesting that the changes induced by METH treatment are due to alterations in K-m and not in the number of DA transport sites. The results from these studies indicate that METH treatment produces a modification in transporter function which may be associated with both the altered uptake and release of [H-3]DA. These changes havebroad implications for the regulation of transporter activity not only because of the relevance to pre-synaptic mechanisms controlling neurotransmission, but also to the importance of the neuronal adaptation that occurs in response to chronic METH exposure. (C) 1998 Elsevier Science B.V.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 19:38:42