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Titolo:
Long-term changes in basal ganglia function after a neurotoxic regimen of methamphetamine
Autore:
Chapman, DE; Hanson, GR; Kesner, RP; Keefe, KA;
Indirizzi:
Univ Utah, Coll Pharm, Dept Pharmacol & Toxicol, Salt Lake City, UT 84112 USA Univ Utah Salt Lake City UT USA 84112 xicol, Salt Lake City, UT 84112 USA Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA Univ Utah Salt LakeCity UT USA 84112 ychol, Salt Lake City, UT 84112 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 2, volume: 296, anno: 2001,
pagine: 520 - 527
SICI:
0022-3565(200102)296:2<520:LCIBGF>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA EXPRESSION; D1 DOPAMINE RECEPTOR; STRIATAL DOPAMINE; SUBSTANCE-P; 6-HYDROXYDOPAMINE LESION; NONHUMAN-PRIMATES; GENE-EXPRESSION; RHESUS-MONKEYS; NMDA RECEPTORS; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Keefe, KA Univ Utah, Coll Pharm, Dept Pharmacol & Toxicol, 30 South 2000 East,Room 201, Salt Lake City, UT 84112 USA Univ Utah 30 South 2000 East,Room 201 Salt Lake City UT USA 84112
Citazione:
D.E. Chapman et al., "Long-term changes in basal ganglia function after a neurotoxic regimen of methamphetamine", J PHARM EXP, 296(2), 2001, pp. 520-527

Abstract

The abuse of psychostimulants, such as methamphetamine (METH), can cause long-lasting deficits in the dopamine (DA) innervation of the striatum. Although the consequences of large DA depletions on basal ganglia function havebeen well characterized, less is known about the alterations associated with smaller depletions, such as those produced by high doses of METH. The purpose of this study was to assess the long-term consequences of METH-induced DA depletion on basal ganglia function. Three weeks after rats were givenmultiple administrations of METH (5-10 mg/kg, four times at 2-h intervals), dose-related decreases in DA tissue content in striatum and tyrosine hydroxylase mRNA in the substantia nigra pars compacta were observed. In situ hybridization histochemistry revealed a selective decrease in preprotachykinin mRNA in striatum, predominately at the highest dose of METH, and no change in striatal preprodynorphin, preproenkephalin, or neurotensin/ neuromedin N mRNAs. Cytochrome oxidase activity was significantly elevated in the entopeduncular nucleus and substantia nigra pars reticulata of METH-treated rats, but not in the striatum, globus pallidus, or subthalamic nucleus, consistent with a selective decrease in striatonigral, but not striatopallidal,neuron function. Additionally, rats treated with a neurotoxic regimen of METH were impaired on a radial maze sequential learning task when tested 3 weeks following METH administration. These data indicate that exposure to a neurotoxic regimen of METH results in long-term changes in striatonigral, but not striatopallidal neuron function and, consequently, altered basal ganglia function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 03:22:32