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lüll Limbic-cortical neuronal damage and the pathophysiology of schizophrenia Csernansky JG; Bardgett MESchizophr Bull 1998[]; 24 (2): 231-48Neurobiological 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.|*Models, Neurological[MESH]|Animals[MESH]|Antipsychotic Agents/pharmacology[MESH]|Brain/drug effects/pathology/physiopathology[MESH]|Disease Models, Animal[MESH]|Disease Progression[MESH]|Dopamine Agents/pharmacology[MESH]|Dopamine/physiology[MESH]|Drug Resistance/physiology[MESH]|Frontal Lobe/physiopathology[MESH]|Glutamic Acid/physiology[MESH]|Hippocampus/injuries/pathology/physiopathology[MESH]|Humans[MESH]|Limbic System/injuries/*pathology/physiopathology[MESH]|Neural Pathways/drug effects/pathology/physiopathology[MESH]|Schizophrenia/drug therapy/etiology/pathology/*physiopathology[MESH]|Severity of Illness Index[MESH] |