Ritalin May Cause Changes In Brain’s Reward Areas; Effects May Overlap With Thos

February 9, 2009

Ritalin May Cause Changes In Brain's Reward Areas; Effects May

Overlap With Those Of Cocaine

ScienceDaily (Feb. 5, 2009) — A common treatment for attention

deficit/hyperactivity disorder, prescribed millions of times a year,

may change the brain in the same ways that cocaine does, a new study

in mice suggests. Research from Rockefeller University shows that

methylphenidate, commonly known as Ritalin, causes physical changes

in neurons in reward regions of mouse brains. In some cases, the

effects overlapped with those of cocaine.

The study highlights the need for more research into

methylphenidate's long-term effects on the brain, the researchers say.

The researchers, led by Yong Kim, senior research associate, and

Greengard, Astor Professor and head of the Laboratory of

Molecular and Cellular Neuroscience, exposed mice to two weeks of

daily injections of cocaine or methylphenidate. They then examined

reward areas of the brain for changes in dendritic spine formation —

related to the formation of synapses and the communication between

nerve cells — and the expression of a protein called delta Fos B,

which has been implicated in the long-term actions of addictive drugs.

Both drugs increased dendritic spine formation and the expression of

delta Fos B; however, the precise patterns of their effects were

distinct. They differed in the types of spines affected, the cells

that were affected and the brain regions. In some cases there was

overlap between the two drugs, and in some cases methylphenidate

produced greater effects than cocaine, for example, on protein

expression in certain regions. Both methylphenidate and cocaine are

in the class of drugs known as psychostimulants.

" Methylphenidate, which is thought to be a fairly innocuous compound,

can have structural and biochemical effects in some regions of the

brain that can be even greater than those of cocaine, " says

Kim. " Further studies are needed to determine the behavioral

implications of these changes and to understand the mechanisms by

which these drugs affect synapse formation. "

Reference: Proceedings of the National Academy of Sciences: February

3, 2009

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