To test this hypothesis and to consider why such a defect would not be expressed until adolescence, two approaches are being used. First, pregnant dams are being exposed to neurotoxic doses of glucocorticoids to simulate a stress response, or ibotenic acid will be stereotaxically applied to superficial laminae of the medial prefrontal cortex of rat pups. The second strategy has involved studies of normal development in human brain to identify whether postnatal ontogenetic changes may trigger the expression of a latent defect in schizophrenia. Finally, rodent investigations are also employed to assess whether long-term administration of either haloperidol or clozapine may induce changes in the glutamate or GABA systems of limbic cortex. Mailman Research Center, McLean Hospital Project Director and Contact.
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GABA A receptor binding in superficial layers of cingulate cortex in schizophrenics. Dopamine immunoreactive axon varicosities form nonrandom contacts with GABAimmunoreactive neurons in rat medial prefrontal cortex. Cellular distribution of dopamine D1 and D2 receptors in rat medial prefrontal cortex.