April 1995

In Pursuit of the Molecular Neuropathology of Schizophrenia-Reply

Author Affiliations

Department of Anatomy and Neurobiology University of California, Irvine Irvine, CA 92717

Arch Gen Psychiatry. 1995;52(4):277-278. doi:10.1001/archpsyc.1995.03950160027006

In reply  Each of the three commentaries on our article1 raises important issues for discussion.Lee and Tobin2 claim a discrepancy between our findings of reduced glutamic acid decarboxylase messenger RNA (GAD mRNA) levels in the prefrontal cortex of schizophrenics and the lack of similar changes in GAD enzyme activity reported by Hanada et al.3 This is not surprising, given the fact that GAD enzyme is unstable and its activity is influenced by confounding factors such as autolysis time4 and cause of death.3,5 Two other studies reported decreased GAD activity in schizophrenics,6,7 but one only found decreased GAD activity in schizophrenics who did not die a sudden death.5 The GAD mRNA is far more resistant to autolysis, and localization by in situ hybridization was successful in all patients and controls included in this study. In the same specimens, staining of GAD enzyme by means

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