News Editor: Renato M.E. Sabbatini, PhD
Brain and Cocaine
For the first time, researchers techniques of positron emission tomography (PET) have observed in human cocaine abusers some of the ways by which cocaine produces its pleasurable effects as they are occurring.
Those studies have suggested that cocaine works in large part by occupying or blocking dopamine transporter (DAT) sites, thereby preventing reuptake of dopamine by the brain cells that release it, which then allows higher concentrations of dopamine to remain available in the brain longer than normal. It is this abnormally long presence of dopamine in the brain that is believed to cause the high and other effects associated with cocaine use.
In another study published in the same issue of Nature, Dr. Volkow and colleagues compared the functioning of the dopamine system in the brains of chronic cocaine users with that in non-users.
Methylphenidate, a stimulant similar to cocaine that increases dopamine responsiveness in the brain, was administered to both the users and non-users. Using the PET technology, researchers obtained brain images that contrasted how the dopamine systems in the two groups responded to the methylphenidate.
They found that, compared to the non-users, the cocaine-dependent group showed reduced dopamine responses to the drug in the striatum, a region of the brain linked to motivation control and reward. At the same time, they found an abnormal increase in the level of dopamine response in the thalamus, a region of the brain that communicates sensory information.
Nature, April 24, 1997.