Pretreatment with a dopamine D1-receptor antagonist prevents metabolic activation by cocaine.
The pharmacological mechanism underlying metabolic activation of the rat extrapyramidal system by acute cocaine was examined using the quantitative 2-deoxyglucose autoradiographic method. Pretreatment with a selective dopamine D1-like receptor antagonist, SCH 23390, prevented cocaine-induced metabolic activation in the entopeduncular nucleus and substantia nigra pars reticulata in a dose-dependent manner. These results suggest that activity in striatonigral circuits is induced by stimulation of D1-like receptors by dopamine in the presence of acute cocaine.
Thomas
W L
WL
Department of Psychiatry, New England Medical Center, Tufts University School of Medicine, Boston, MA 02111, USA.
Cooke
E S
ES
Hammer
R P
RP
D000818:Animals; D001345:Autoradiography; D001552:Benzazepines / Q000493:pharmacokinetics / Q000494:pharmacology*; D001711:Biotransformation; D003042:Cocaine / Q000037:antagonists & inhibitors*; D003847:Deoxyglucose; D004305:Dose-Response Relationship, Drug; D005116:Extrapyramidal Tracts / Q000187:drug effects*; D008297:Male; D018696:Neuroprotective Agents / Q000493:pharmacokinetics / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors*
D001552:Benzazepines; D018696:Neuroprotective Agents; D017447:Receptors, Dopamine D1; D003847:Deoxyglucose; D003042:Cocaine