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Schizophrenia Bulletin 1998 24(2):231-248;
© 1998 by Oxford University Press and the Maryland Psychiatric Research Center (MPRC)
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© Oxford University Press

Limbic-Cortical Neuronal Damage and the Pathophysiology of Schizophrenia

John G. Csernansky, M.D. and Mark E. Bardgett, Ph.D.
Gregory B. Couch Professor of Psychiatry and Neurobiology, Washington University School of Medicine, and Medical Director, Metropolitan St. Louis Psychiatric Center St. Louis, MO
Research Assistant Professor of Neurobiology in Psychiatry, Washington University School of Medicine St. Louis, MO

Reprint requests should be sent to Dr. J.G. Csernansky, Dept. of Psychiatry, Box 8134, Washington University School of Medicine, St. Louis, MO 63110

Neurobiological studies of patients with schizophrenia suggest that abnormalities of both anatomy and function occur in limbic-cortical structures. An anatomical circuit links the functioning of the ventral striatum (i.e., nucleus accumbens) with the hippocampus and other limbic-cortical structures where neurobiological abnormalities have been found. In animals, lesions of limbic-cortical neurons cause decreases in glutamatergic input to the nucleus accumbens and are also associated with decreases in presynaptic dopamine release, increases in the density of D2-like dopamine receptors, and insensitivity to the actions of dopamine antagonists such as haloperidol. These experiments suggest a plausible pathophysiology of schizophrenia, in that schizophrenic symptoms may be caused by an abnormal dopaminergic state brought about by a primary limbic-cortical lesion and deficits in glutamatergic inputs to the ventral striatum.

Keywords: Hippocampus / dopamine / antipsychotic drugs


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