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Biological Chemistry

Gaining control of drug cravings

February 20, 2006 | A version of this story appeared in Volume 84, Issue 8

Initial drug use temporarily activates reward circuits involving dopamine in the brain's ventral tegmental area (VTA). Habitual use leads to long-term activation of these circuits, which "rewires" the brain and results in more intense drug craving. Two research groups that study these changes have reported results that could lead to treatments for drug addiction. University of California, San Francisco, neurologist Antonello Bonci and colleagues found that cocaine causes the brain peptide orexin A to produce long-lasting changes in dopamine neurons in the VTA (Neuron 2006, 49, 589). Blocking orexin A prevents these changes and inhibits the development of cocaine craving in rats. University of Saskatchewan neuropsychiatrist Xia Zhang led a team that focused on nicotine and Δ9-tetrahydrocannabinol (THC), the active ingredient in marijuana (Nat. Med., published online Feb. 12, dx.doi.org/10.1038/nm1349). These drugs activate dopamine neurons in the VTA. The group determined that a complex formed between the brain enzyme PTEN and serotonin receptors also regulates dopamine neurons. Disruption of this complex with a synthetic peptide stops nicotine and THC from activating the dopamine neurons and prevents drug-induced euphoria in rats.

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