Cocaine, reward, movement
and monoamine transporters

Uhl GR, Hall FS, Sora I.
Molecular Neurobiology Branch,
NIDA-IRP, NIH, Baltimore, MD 21224, USA.
Mol Psychiatry 2002 Jan;7(1):21-6


Recent evidence enriches our understanding of the molecular sites of action of cocaine reward and locomotor stimulation. Dopamine transporter blockade by cocaine appears a sufficient explanation for cocaine-induced locomotion. Variation in DAT appears to cause differences in locomotion without drug stimulation. However, previously-held views that DAT blockade was the sole site for cocaine reward have been replaced by a richer picture of multitransporter involvement with the rewarding and aversive actions of cocaine. These new insights, derived from studies of knockout mice with simultaneous deletions and/or blockade of multiple transporters, provide a novel model for the rewarding action of this heavily-abused substance and implicate multiple monoamine systems in cocaine's hedonic activities.

Delta FosB
Oral cocaine
Dopaminergic flies?
Dopaminergic agents
The coke-craving brain
Cocaine and depression
Cocaine and the lonely rat
Monoamines, cocaine and rats
A disease of the reward centers?
Cocaine highs and the olfactory tubercle
Does cocaine use damage the pleasure centers?
Dopamine/noradrenaline vs serotonin releasers to treat cocaine dependence

01 02 03 04 05 06 07 08 09 10 11 12
13 14 15 16 17 18 19 20 21 22 23 24

Future Opioids
BLTC Research
Wirehead Hedonism
Utopian Pharmacology
The Hedonistic Imperative
When Is It Best to Take Crack Cocaine?

swan image
The Good Drug Guide
The Responsible Parent's Guide To
Healthy Mood Boosters For All The Family