SAN DIEGO -- Scientists at the University at Buffalo have shown that the drug methylphenidate, the generic form of Ritalin, which physicians have considered to have only short-term effects, appears to initiate changes in brain function that remain after the therapeutic effects have dissipated.

The changes appear to be similar to those that occur with other stimulant drugs such as amphetamine and cocaine, said Joan Baizer, Ph.D., UB professor of physiology and biophysics and senior author of the study. Results of the research were presented here today (Nov. 11, 2001) at the annual meeting of the Society for Neuroscience.

"Clinicians consider Ritalin to be short-acting," said Baizer. "When the active dose has worked its way through the system, they consider it 'all gone.' Our research with gene expression in an animal model suggests that it has the potential for causing long-lasting changes in brain cell structure and function." Ritalin is the drug of choice for the treatment of attention deficit disorder in children.

Baizer stated, however, that while the neuronal changes are similar to those seen with cocaine and other psychoactive drugs, it does not seem that methylphenidate in very low doses, as used therapeutically, produces much potential for drug abuse.

"Children have been given Ritalin daily for many years, and it is extremely effective and beneficial, but it's not quite as simple as a short-acting drug," Baizer said. "We need to look at it more closely." Baizer added: "Ritalin does appear to be safe when used properly, but it is still important to ask what it is doing in the brain."

Previous work in other laboratories has shown that high doses of amphetamine and cocaine switch on certain genes called "immediate early genes" in particular brain cells and that this action causes changes in some aspects of nerve cell function. One of those genes is called "c-fos." Amphetamine and cocaine both cause c-fos activity in the st
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Contact: Lois Baker
ljbaker@buffalo.edu
716-645-5000 x 1417
University at Buffalo
11-Nov-2001

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