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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1990-6-27
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pubmed:abstractText |
The cocaine-antagonist effects of SCH 39166, which selectively blocks D1 dopamine receptors, were compared with those of YM 09151-2, a selective D2 receptor blocker, and flupenthixol, a nonselective blocker of both dopamine receptor subtypes. Squirrel monkeys were studied under a fixed-interval schedule of stimulus-shock termination, and the effects of cumulative doses of cocaine were determined alone and after pretreatment with each dopamine receptor blocker. When administered alone, cocaine (0.01-1.78 mg/kg, IV) had biphasic effects on responding: intermediate doses increased response rate, whereas higher doses decreased response rate. The ED50 for cocaine (average does that produced a half-maximal increase in response rate) was 0.04 mg/kg. Pretreatment with SCH 39166 (0.03 and 0.1 mg/kg, IV) resulted in surmountable antagonism of both the rate-increasing and rate-decreasing effects of cocaine, the ED50 being increased by as much as 13-fold. Similar effects were observed after pretreatment with YM 09151-2 (0.001 and 0.003 mg/kg, IV) and flupenthixol (0.01 and 0.03 mg/kg, IV), which respectively produced up to a 13-fold and 32-fold increase in ED50. There also was evidence for reciprocal antagonism of the rate-decreasing effects of the three dopamine receptor blockers by cocaine. The results suggest a prominent role for D1 as well as D2 dopamine receptors in mediating the effects of cocaine on schedule-controlled behavior.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antipsychotic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Benzamides,
http://linkedlifedata.com/resource/pubmed/chemical/Benzazepines,
http://linkedlifedata.com/resource/pubmed/chemical/Cocaine,
http://linkedlifedata.com/resource/pubmed/chemical/Flupenthixol,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Dopamine,
http://linkedlifedata.com/resource/pubmed/chemical/Sch 39166,
http://linkedlifedata.com/resource/pubmed/chemical/nemonapride
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pubmed:status |
MEDLINE
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pubmed:issn |
0033-3158
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
101
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
142-5
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1971446-Animals,
pubmed-meshheading:1971446-Antipsychotic Agents,
pubmed-meshheading:1971446-Behavior, Animal,
pubmed-meshheading:1971446-Benzamides,
pubmed-meshheading:1971446-Benzazepines,
pubmed-meshheading:1971446-Cocaine,
pubmed-meshheading:1971446-Conditioning, Operant,
pubmed-meshheading:1971446-Dose-Response Relationship, Drug,
pubmed-meshheading:1971446-Flupenthixol,
pubmed-meshheading:1971446-Male,
pubmed-meshheading:1971446-Receptors, Dopamine,
pubmed-meshheading:1971446-Reinforcement Schedule,
pubmed-meshheading:1971446-Saimiri
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pubmed:year |
1990
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pubmed:articleTitle |
Antagonism of behavioral effects of cocaine by selective dopamine receptor blockers.
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pubmed:affiliation |
Harvard Medical School, New England Regional Primate Research Center, Southborough, MA 01772.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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