Wednesday, April 3, 2013

Study shows relationship between cocaine-induced brain deficits in prefrontal cortex and cocaine-seeking


Could drug addiction treatment of the future be as simple as an on/off switch in the brain? A study in rats has found that stimulating a key part of the brain reduces compulsive cocaine-seeking and suggests the possibility of changing addictive behavior generally. The study, published in Nature, was conducted by scientists at the Intramural Research Program of the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, and the University of California, San Francisco.


"This exciting study offers a new direction of research for the treatment of cocaine and possibly other addictions," said NIDA Director Dr. Nora D. Volkow. "We already knew, mainly from human brain imaging studies, that deficits in the prefrontal cortex are involved in drug addiction. Now that we have learned how fundamental these deficits are, we feel more confident than ever about the therapeutic promise of targeting that part of the brain."


Compulsive drug-taking, despite negative health and social consequences, has been the most difficult challenge in human drug addiction. NIDA researchers used an animal model of cocaine addiction, in which some rats exhibited addictive behavior by pushing levers to get cocaine even when followed by a mild electric shock to the foot. Other rats did not exhibit addictive responses.


The NIDA scientists compared nerve cell firing patterns in both groups of rats by examining cells from the prefrontal cortex. They determined that cocaine produced greater functional brain deficits in the addicted rats. Scientists then used optogenetic techniques on both groups of rats -- essentially shining a light onto modified cells to increase or lessen activity in that part of the brain. In the addicted rats, activating the brain cells (thereby removing the deficits) reduced cocaine-seeking. In the non-addicted rats, deactivating the brain cells (thereby creating the deficits) increased compulsive cocaine seeking.



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