Altered Glutamatergic and GABAergic Mechanisms in the Cingulate Cortex of the Schizophrenic Brain

Abstract

The arthcle in this issue of theArchivesentitled "Glutamate Receptor Dysfunction and Schizophrenia" by Olney and Farber¹presents a provocative hypothesis concerning the role of<i>N</i>-methyl-Daspartate (NMDA)—mediated glutamatergic dysfunction in the pathophysiology of schizophrenia. The ideas have evolved out of Dr Olney's studies of phencyclidine (PCP)-induced neurotoxicity in the cingulate and retrosplenial cortices of the rat brain and his subsequent efforts to elucidate the neuropharmacological characteristics of this effect. It is timely that the authors have brought together this body of work and that they have used it to model several key questions concerning schizophrenia. Toward this end, the article focused primarily on animal investigations to support the details of the model circuit they presented in Figure 4. It is noteworthy that other data from postmortem studies can corroborate several aspects of the Olney and Farber model, particularly the central idea that there may be