Limbic-cortical neuronal damage and the pathophysiology of schizophrenia

John G. Csernansky*, Mark E. Bardgett

*Corresponding author for this work

Research output: Contribution to journalReview article

88 Scopus citations


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 languageEnglish (US)
Pages (from-to)231-248
Number of pages18
JournalSchizophrenia bulletin
Issue number2
StatePublished - Jan 1 1998


  • Antipsychotic drugs
  • Dopamine
  • Hippocampus

ASJC Scopus subject areas

  • Psychiatry and Mental health

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