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Quantitation of GAD67 Gene Expression in Prefrontal Cortex of Schizophrenia Patients Using the iCycler iQ Detection System and Molecular Beacons, Rev A

Stella Dracheva, Bronx VA Medical Center, Psychiatry Research,
130 West Kingsbridge Road, Bronx, NY 10468 USA


Introduction
Schizophrenia is a severe mental illness that afflicts about 1% of the population (Strange 1992). Patients experience a variety of symptoms that have been divided into subgroups of positive symptoms (e.g., thought disorder, abnormal beliefs and experiences) and negative symptoms (e.g., deficiency of speech, loss of emotional response, reduced motor function). The etiology and pathophysiology of schizophrenia have been the focus of intensive research for decades. Convergent lines of evidence indicate that dysfunction of a specific area of the cerebral cortex the dorsolateral prefrontal cortex represents one of the central features of the pathophysiology of schizophrenia (Bunney and Bunney 2000). A synthesis of results from in vivo imaging and postmortem studies (Lewis et al. 1999) also suggests that prefrontal cortex dysfunction may be related to abnormalities in the connectivity between neurons in this region that are likely to involve GABAergic interneurons (neurons that synthesize and release the major inhibitory neurotransmitter in the brain, γ-aminobutyric acid or GABA). The synthesis of GABA is catalyzed by the enzyme glutamic acid decarboxylase (GAD). Molecular cloning studies have shown that in the adult brain, GAD exists in 2 isoforms, called GAD65 and GAD67, which are the products of 2 independently regulated genes. GAD65 and GAD67 are coexpressed in GABAergic neurons. Gene lesioning studies in mice (Condie et al. 1997, Kash et al. 1997) suggest that GAD67 is the major isoform and is responsible for the maintenance of basal GABA
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