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Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter.

Nature | Feb 15, 1996

http://www.ncbi.nlm.nih.gov/pubmed/8628395

Disruption of the mouse dopamine transporter gene results in spontaneous hyperlocomotion despite major adaptive changes, such as decreases in neurotransmitter and receptor levels. In homozygote mice, dopamine persists at least 100 times longer in the extracellular space, explaining the biochemical basis of the hyperdopaminergic phenotype and demonstrating the critical role of the transporter in regulating neurotransmission. The dopamine transporter is an obligatory target of cocaine and amphetamine, as these psychostimulants have no effect on locomotor activity or dopamine release and uptake in mice lacking the transporter.

Pubmed ID: 8628395 RIS Download

Mesh terms: Amphetamine | Animals | Carrier Proteins | Cell Line | Cocaine | Dopamine | Dopamine Plasma Membrane Transport Proteins | Dynorphins | Enkephalins | Female | Gene Expression Regulation | Gene Targeting | Locomotion | Male | Membrane Glycoproteins | Membrane Transport Proteins | Mice | Mice, Inbred C57BL | Mice, Knockout | Nerve Tissue Proteins | Protein Precursors | Rats

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Mouse Genome Informatics (Data, Gene Annotation)

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