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Genetically altered mice no longer like cocaine

ears to be a suppressant, not a stimulant," Gu said.

In previous work, other scientists studied mice that lacked a dopamine transporter. Since cocaine's key target was missing in these mice, the researchers thought that the drug wouldn't trigger a high. They were wrong. This led to the proposal that there may be redundant reward pathways for cocaine reward.

"Deleting the dopamine transporter itself caused tremendous changes in the mouse brain," Gu said. "It's possible that, somehow, the animals' brains rewired themselves and, as a result, the mice still felt the effects of cocaine."

The current study suggests that cocaine's blockade of dopamine transporters is still required in order to produce a high in normal mice.

Gu said the next step is to screen for compounds that could produce the same effect that the genetic modifications did in this study.

"We hope to find certain drugs that prevent cocaine from binding to transporters, but that still allow the transporter protein to carry the dopamine back to the neuron," he said.

Gu conducted the study with researchers from Ohio State, the University of Tennessee College of Medicine, in Memphis, and Yale University.


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Contact: Howard Gu
Gu.37@osu.edu
614-292-1324
Ohio State University
31-May-2006


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