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Titolo:
Evidence against an essential role of endogenous brain dopamine in methamphetamine-induced dopaminergic neurotoxicity
Autore:
Yuan, J; Callahan, BT; McCann, UD; Ricaurte, GA;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Neurol, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 ychiat, Baltimore, MD 21205 USA
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 5, volume: 77, anno: 2001,
pagine: 1338 - 1347
SICI:
0022-3042(200106)77:5<1338:EAAERO>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSITRON-EMISSION-TOMOGRAPHY; HYDROXYL RADICAL FORMATION; STRIATAL DOPAMINE; BODY-TEMPERATURE; ENVIRONMENTAL-TEMPERATURE; SEROTONIN NEUROTOXICITY; PHARMACOLOGICAL AGENTS; OXIDATIVE STRESS; C-11 WIN-35,428; RAT STRIATUM;
Keywords:
dopamine; methamphetamine; alpha-methyl-p-tyrosine; neurotoxicity; reserpine; temperature;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Ricaurte, GA Johns Hopkins Med Inst, Dept Neurol, 5501 Hopkins Bayview Circle,Rm 5B71E,Baltimore, MD 21224 USA Johns Hopkins Med Inst 5501 Hopkins Bayview Circle,Rm 5B71E Baltimore MD USA 21224
Citazione:
J. Yuan et al., "Evidence against an essential role of endogenous brain dopamine in methamphetamine-induced dopaminergic neurotoxicity", J NEUROCHEM, 77(5), 2001, pp. 1338-1347

Abstract

The present studies examined the role of endogenous dopamine (DA) in methamphetamine (METH)-induced dopaminergic neurotoxicity while controlling for temperature-related neuroprotective effects of the test compounds, reserpine and alpha -methyl-p-tyrosine (AMPT). To determine if the vesicular pool of DA was essential for the expression of METH-induced DA neurotoxicity, reserpine (3 mg/kg, given iintraperitoneally 24-26 h prior to METH) was given prior to a toxic dose regimen of METH. Despite severe striatal DA deficits during the period of METH exposure, mice treated with reserpine prior to METH developed long-term reductions in striatal DA axonal markers, suggestingthat vesicular DA stores were not crucial for the development of METH neurotoxicity, but leaving open the possibility that cytoplasmic DA might be involved. To evaluate this possibility, cytoplasmic DA stores were depleted with AMPT prior to METH administration. When this study was carried out at 28 degreesC, complete neuroprotection was observed, likely due to lingering effects on core temperature because when the same study was repeated at 33 degreesC (to eliminate AMPT's hypothermic effect in METH-treated animals), the previously observed neuroprotection was no longer evident. In the thirdand final set of experiments, mice were pretreated with a combination of reserpine and AMPT, to deplete both vesicular and cytoplasmic DA pools, and to reduce striatal DA levels to negligible values during the period of METHadministration (< 0.05%). When core temperature differences were eliminated by raising ambient temperature, METH-induced DA neurotoxic changes were evident in mice pretreated with reserpine and AMPT. Collectively, these findings bring into question the view that endogenous DA plays an essential role in METH-induced DA neurotoxicity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 07:27:57