Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
REPEATED QUINPIROLE TREATMENT - LOCOMOTOR-ACTIVITY, DOPAMINE SYNTHESIS, AND EFFECTS OF SELECTIVE DOPAMINE ANTAGONISTS
Autore:
ROWLETT JK; MATTINGLY BA; BARDO MT;
Indirizzi:
MOREHEAD STATE UNIV,DEPT PSYCHOL MOREHEAD KY 40351 MOREHEAD STATE UNIV,DEPT PSYCHOL MOREHEAD KY 40351 UNIV KENTUCKY,DEPT PSYCHOL LEXINGTON KY 40506
Titolo Testata:
Synapse
fascicolo: 3, volume: 20, anno: 1995,
pagine: 209 - 216
SICI:
0887-4476(1995)20:3<209:RQT-LD>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
BEHAVIORAL SENSITIZATION; REPEATED APOMORPHINE; AUTORECEPTOR SUBSENSITIVITY; RECEPTOR STIMULATION; CHRONIC AMPHETAMINE; RAT-BRAIN; SENSITIVITY; AGONISTS; RELEASE; CLONING;
Keywords:
BEHAVIORAL SENSITIZATION; 3,4-DIHYDROXYPHENYLALANINE (DOPA); SCH 23390; ETICLOPRIDE; NIGROSTRIATAL PATHWAY; MESOLIMBIC PATHWAY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
J.K. Rowlett et al., "REPEATED QUINPIROLE TREATMENT - LOCOMOTOR-ACTIVITY, DOPAMINE SYNTHESIS, AND EFFECTS OF SELECTIVE DOPAMINE ANTAGONISTS", Synapse, 20(3), 1995, pp. 209-216

Abstract

Repeated treatment with the non-selective dopamine agonist apomorphine results in behavioral sensitization and enhanced dopamine synthesis in dopamine projection fields. To examine the role of D-2-type dopamine receptors in modulating these effects, the present experiment assessed the effects of repeated treatment with the D-2-type agonist quinpirole on locomotor activity and dopamine synthesis. In the first experiment, rats were treated with vehicle or one of two doses (0.3 or 3.0 mg/kg) of quinpirole for 8 days. Daily measures of locomotor activity revealed an initial suppression of activity produced by quinpirole whichdissipated over the 8 days of treatment. A trend for an increase in activity for 3.0 mg/kg quinpirole compared to vehicle was obtained on day 8. Twenty-four hours after cessation of treatment, dopamine synthesis, measured as accumulation of 3,4-dihydroxyphenylalanine (DOPA) after treatment with the DOPA decarboxylase inhibitor NSD-1015, was enhanced in the striatum, but not nucleus accumbens-olfactory tubercle (NAOT) or ventral mesencephalon (VM). In Experiment 2, rats were treated for 8 days with vehicle, 3.0 mg/kg quinpirole or the D-1 antagonist SCH 23390 (0.5 mg/kg) in a two (vehicle or quinpirole) x two (vehicle or SCH 23390) design. Quinpirole-alone treatment resulted in a reduction of the locomotor suppressant effects of the drug. SCH 23390-alone and quinpirole-SCH 23390 combined treatment resulted in decreased activity compared to the vehicle control group that did not change across days. DOPA accumulation was enhanced in the striatum and NAOT after quinpirole treatment; however, SCH 23390 had no effect. In Experiment 3, ratswere treated for 10 days with vehicle, 3.0 mg/kg quinpirole or the D-2 antagonist eticlopride (1.0 mg/kg) in a two (vehicle or quinpirole) x two (vehicle or eticlopride) design. As in the first two experiments, repeated quinpirole-alone treatment resulted in a reduction of the locomotor suppressant effects of the drug; however, locomotor activity in this group was enhanced compared to vehicle controls on day 10. Eticlopride-alone and eticlopride-quinpirole treated rats had suppressed locomotor activity across the 10 days. DOPA accumulation was enhanced by both repeated quinpirole and repeated eticlopride treatment in the striatum and NAOT. DOPA accumulation in eticlopride-quinpirole treatedrats was not different from vehicle control levels in the NAOT, whileno significant difference was obtained between the eticlopride-alone and eticlopride-quinpirole groups in the striatum. The locomotor activity data suggest that repeated quinpirole treatment results in tolerance to the locomotor suppressant effect of the drug. Evidence for sensitization was obtained in two out of three of the experiments. These results suggest that enhanced dopamine synthesis after repeated non-selective dopamine agonist treatment is modulated by D-2-type dopamine receptors. (C) 1995 Wiley-Liss, Inc.

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