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   <subfield code="a">Linseman</subfield>
   <subfield code="D">M.</subfield>
   <subfield code="u">Biobehavioral Studies Department, Addiction Research Foundation, 33 Russell Street, M5S 2S1, Toronto, Canada</subfield>
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   <subfield code="a">Effects of dopaminergic agents on alcohol consumption by rats in a limited access paradigm</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[M. Linseman]</subfield>
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   <subfield code="a">The effects of several dopaminergic drugs on alcohol consumption were studied in free-feeding rats using a limited access paradigm. Ascending doses of amphetamine (0.1, 0.3 and 1.0 mg/kg), haloperidol (0.1, 0.3 and 1.0 mg/kg), SKF 38 393 (a D1 receptor agonist − 0.3, 1.0 and 3.0 mg/kg), quinpirole (LY 171 555, a D2 receptor agonist − 0.03, 0.1 and 0.3 mg/kg), SCH 23 390 (a D1 receptor blocker, 0.003, 0.01, 0.03 and 0.1 mg/kg) and spiperone (a D2 receptor blocker, 0.003, 0.01, 0.03 and 0.1 mg/kg) were administered IP to rats approximately 30 min prior to their 1-h per day access to alcohol. Each dose was administered for 5 successive days, and the effects of the drugs were compared to those of respective saline or 0.4% lactic acid solution controls. Although there was an overall significant dose effect of amphetamine on alcohol consumption, no single dose altered alcohol consumption significantly from baseline. SKF 38 393 specifically decreased alcohol consumption at the highest dose of 3 mg/kg. Quinpirole significantly increased water consumption at the highest dose but had no effect on alcohol consumption. The antagonist haloperidol decreased alcohol consumption but only at doses that also reduced water consumption. The specific antagonists SCH 23 390 and spiperone decreased water consumption at the highest doses tested without modifying alcohol consumption. Taken together, these data suggest that dopamine does not play as critical a role in mediating the reinforcing effects of alcohol (insofar as they are reflected by alcohol consumption) as it does in relation to other psychoactive drugs, particularly the psychomotor stimulants.</subfield>
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   <subfield code="a">Alcohol</subfield>
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   <subfield code="a">Ethanol</subfield>
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   <subfield code="a">Drinking</subfield>
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   <subfield code="a">Self-administration</subfield>
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   <subfield code="a">Dopamine</subfield>
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