Project Summary

David A. Baker, Ph.D. (Young Investigator 2004) of Marquette University, notes that people with schizophrenia show irregular activity in the prefrontal cortex, and that drugs that block the NMDA class of glutamate receptors, such as phencyclidine (PCP), produce a schizophrenia-like state in humans. Recent evidence shows that group 2/3 metabotrobic glutamate receptors, another type of glutamate receptor, reverse PCP-induced cognitive defects in rats given PCP. Cystine-glutamate antiporters regulate these glutamate receptors and the synthesis of the essential antioxidant glutathione, key to brain cell survival. Individuals with schizophrenia exhibit reduced glutathione levels, suggesting the cystine-glutamate antiporters may be altered. In his proposal, Dr. Baker will examine if PCP treatment of rats alters cystine-glutamate antiporter activity and whether drugs that increase the antiporters can reverse cognitive deficits produced by PCP. Results could lead to new understanding and treatments for schizophrenia exploiting the antiporter pathway.

Program Area: SCHIZOPHRENIA/PSYCHOTIC DISORDERS\Schizophrenia

Search Again