Prenatal exposure to cocaine reduces dopaminergic D1-mediated motor function but spares the enhancement of learning by amphetamine in rabbits.
Simansky
K J
KJ
Department of Pharmacology, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19129, USA. Simansky@AUHS.EDU
Baker
G
G
Kachelries
W J
WJ
Hood
H
H
Romano
A G
AG
Harvey
J A
JA
D000161:Acoustic Stimulation; D000818:Animals; D001245:Association Learning / Q000187:drug effects*; D001552:Benzazepines / Q000494:pharmacology; D001767:Blinking / Q000187:drug effects / Q000502:physiology; D002375:Catalepsy / Q000209:etiology / Q000503:physiopathology; D003042:Cocaine / Q000633:toxicity*; D003216:Conditioning, Operant / Q000187:drug effects; D003913:Dextroamphetamine / Q000494:pharmacology; D005260:Female; D008124:Locomotion / Q000187:drug effects; D008297:Male; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D009541:Nictitating Membrane; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011817:Rabbits; D017447:Receptors, Dopamine D1 / Q000502:physiology*; D012727:Sex Characteristics; D013239:Stereotyped Behavior / Q000187:drug effects
D001552:Benzazepines; D017447:Receptors, Dopamine D1; D003042:Cocaine; D003913:Dextroamphetamine