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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-10-23
pubmed:abstractText
Interactions at the behavioral level between dopamine (DA) and opioid receptors in the mammalian brain have been amply demonstrated. Considering the pivotal role for DA receptors in the pharmacotherapy of Parkinson's disease (PD), these interactions might be clinically relevant. Therefore, in the present study the effects of the opioid antagonist naltrexone and agonist morphine on D1 and D2 receptor induced stimulation of motor behavior in the unilateral MPTP monkey model (n = 5) of PD were investigated. The results show that both naltrexone and morphine [0.1-1.0 mg/kg; intramuscular injection (IM)] inhibited D2 receptor stimulated contralateral rotational behavior and hand use induced by administration of quinpirole (LY 171555; 0.01 mg/kg, IM) in a dose-related way. However, no effects of these opioid drugs were observed on D1 receptor stimulated contralateral rotational behavior and hand use induced by administration of SKF 81297 (0.3 mg/kg, IM). Interestingly, the action of the alleged preferential mu-receptor antagonist naltrexone was mimicked by the selective delta-opioid antagonist naltrindole (0.5 mg/kg, IM). From this study it is concluded that in a non-human primate model of PD, alteration of opioid tonus leads to modulation of D2 receptor but not D1 receptor controlled motor behavior. The possible underlying mechanisms and clinical relevance of these findings are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0033-3158
pubmed:author
pubmed:issnType
Print
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
451-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Morphine and naltrexone modulate D2 but not D1 receptor induced motor behavior in MPTP-lesioned monkeys.
pubmed:affiliation
Graduate School Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit, Department of Neurology, Medical Faculty, The Netherlands.
pubmed:publicationType
Journal Article