Rat Modeling for GABA Defects

Postmortem studies of schizophrenia conducted over the past 15 years have demonstrated alterations in various markers for the g‐aminobutyric acid (GABA) system that are consistent with a reduction of inhibitory modulation in the limbic lobe. These changes show a preferential distribution in layer II of the anterior cingulate cortex (ACCx) and sectors CA3 and CA2 of the hippocampus. Both of these sites receive a rich projection from the basolateral amygdala (BLa), and this has suggested this latter region might play a pivotal role in the induction of abnormalities in the limbic lobe of schizophrenics. To explore this possibility, a ‘‘partial’’ rodent model for neural circuitry abnormalities in schizophrenia has been applied to the study of limbic lobe circuitry in this disorder. When the GABAA receptor antagonist, picrotoxin (PICRO), is stereotaxically infused into the BLa of awake, freely moving rats, reductions in the number of GABA cells have been