Abstract
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.
Original language | English (US) |
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Pages (from-to) | 231-248 |
Number of pages | 18 |
Journal | Schizophrenia bulletin |
Volume | 24 |
Issue number | 2 |
DOIs | |
State | Published - 1998 |
Keywords
- Antipsychotic drugs
- Dopamine
- Hippocampus
ASJC Scopus subject areas
- Psychiatry and Mental health