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Titolo:
PROPOSED ANIMAL-MODEL OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER
Autore:
KOSTRZEWA RM; BRUS R; KALBFLEISCH JH; PERRY KW; FULLER RW;
Indirizzi:
E TENNESSEE STATE UNIV,QUILLEN DISHNER COLL MED,DEPT PHARMACOL JOHNSON CITY TN 37614 E TENNESSEE STATE UNIV,QUILLEN DISHNER COLL MED,MED EDUC SECT,DIV MEDCOMP JOHNSON CITY TN 37614 L WARYNSKI SILESIAN MED ACAD,DEPT PHARMACOL PL-41808 ZABRZE POLAND ELI LILLY & CO,LILLY RES LABS,LILLY CORP CTR INDIANAPOLIS IN 46285
Titolo Testata:
Brain research bulletin
fascicolo: 2, volume: 34, anno: 1994,
pagine: 161 - 167
SICI:
0361-9230(1994)34:2<161:PAOAHD>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPLETING BRAIN-LESIONS; MESOSTRIATAL SEROTONERGIC PATHWAYS; NEONATAL 6-OHDA-LESIONED RATS; D-1 DOPAMINE-RECEPTORS; LOCOMOTOR-ACTIVITY; 5-HYDROXYINDOLEACETIC ACID; D-AMPHETAMINE; BEHAVIORAL-RESPONSES; NUCLEUS ACCUMBENS; HOMOVANILLIC-ACID;
Keywords:
HYPERLOCOMOTION; 6-HYDROXYDOPAMINE; DOPAMINE; SEROTONIN; 5,7-DIHYDROXYTRYPTAMINE; AMPHETAMINE; ORAL ACTIVITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
R.M. Kostrzewa et al., "PROPOSED ANIMAL-MODEL OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER", Brain research bulletin, 34(2), 1994, pp. 161-167

Abstract

Dopamine (DA) neurons are implicated in the hyperlocomotion of neonatal 6-hydroxydopamine (6-OHDA)-lesioned rats, an animal model of attention deficit hyperactivity disorder (ADHD). Because serotonin (5-HT) neurons mediate some DA agonist effects, we investigated the possible role of 5-HT neurons on locomotor activity. Rats were treated at 3 days after birth with vehicle or 6-OHDA (134 mu g ICV; desipramine pretreatment, 20 mg/kg IP, 1 h), and at 10 weeks with vehicle or 5,7-dihydroxytryptamine (5,7-DHT; 75 mu g ICV; pretreatment with desipramine and pargyline, 75 mg/kg IP, 30 min), to destroy DA and/or 5-HT fibers. Intense spontaneous hyperlocomotor activity was produced in rats lesioned with both 6-OHDA and 5,7-DHT. Locomotor time in this group was 550 +/- 17 s in a 600 s session, vs. 127 +/- 13 s in the 6-OHDA group and <75 s in 5,7-DHT and intact control groups (p < 0.001). Oral activity dose-effect curves established that 5,7-DHT attenuated DA D-1 receptor supersensitivity and further sensitized 5-HT2C, receptors. Acute treatment with dextroamphetamine (0.25 mg/kg SC) reduced locomotor time in 6-OHDA+5,7-DHT-lesioned rats to 76 +/- 37 s (p < 0.001). Striatal DA was reduced by 99% and 5-HT was reduced by 30% (vs. 6-OHDA group). Becausecombined 6-OHDA (to neonates) and 5,7-DHT (to adults) lesions produceintense hyperlocomotion that is attenuated by amphetamine, we proposethis as a new animal model of ADHD. The findings suggest that hyperactivity in ADHD may be due to injury or impairment of both DA and 5-HT neurons.

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Documento generato il 02/07/20 alle ore 22:21:12