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Gene-Altered Mouse May Provide New Insights To Parkinson's Disease, Substance Abuse And Schizophrenia

ystem, the body has evolved a precise system for regulating them.

This neurotransmission system involves two main elements: receptors and transporters. Receptors are the molecular "locks" on nerve cells that receive a neurotransmitter "key," causing a neuron to fire a nerve impulse. Transporters are "pumps" on the surface of the transmitting neuron that recycle neurotransmitters back to the nerve cell, to prepare for the next burst.

The neurotransmitter dopamine is stored in tiny hollow spheres, called vesicles, within synaptic "bulbs," which are tiny buds on the nerve cell's surface. When a nerve impulse reaches a bulb, the transmitting neuron releases a flood of dopamine into the narrow space between neurons, called the synapse. When the dopamine reaches the receiving neuron, it binds to specific dopamine receptors, thereby triggering a response in that neuron. Almost immediately, the dopamine transporter scavenges excess dopamine from the synapse to terminate the signal.

It is this dopamine transporter protein that Caron and his colleagues knocked out by disrupting the gene that encodes its production in mice. The resulting mice have no functional dopamine transporter, which means dopamine signals flood the brain and can't be shut off. Depending on where in the brain such overstimulation occurs, it may cause the temporary "high" perceived by cocaine or amphetamine addicts or the permanent and severe delusions experienced by schizophrenics. On the other hand, the lack of dopamine in the brain's motor areas produces the symptoms of Parkinson's disease.

"Virtually every addicting substance appears to modify the dopamine system, implying it may have a central role in addiction," said Alan I. Leshner, director of the National Institute on Drug Abuse (NIDA). "This finding provides a fundamentally new scientific tool in the arsenal to understand and ultimately break the addictive power of drugs."

Caron said the research "poi
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Contact: Karyn Hede George
georg016@mc.duke.edu
919-660-1301
Duke University
29-Apr-1996


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