The evaluation of the differential neuroprotective action of antipsychotics, objectivized through the alteration of hippocampal and prefrontal structures in an experimental study at Common Wistar rats. The neurobiological model of the glucorticoid aggression is validated on the animal model for stress.

We formed 10 study lots each constitued of 5 male adults rats, weighting 200-250 g, held through the study duration (10 days) in temperature, humidity, food and ambient stressless conditions. The studied substancies were administrated intraperitoneal, daily, for 10 days, saline solution equivalent to: olanzapine (0.15mg/kg/day) and ziprasidone (1.25mg/kg/day) single dose at 20:00 hours and haloperidole (0.20mg/kg/day), dexametasone (0.20mg/kg/day) and sulpiride (8mg/kg/day) in two equal doses, at a 12 hour interval (08:00 – 20:00).

The rats were sacrificed during the 10th day, at 6 hours after the last substance administration. The sample brain was histopathologically processed and studied with optical microscopy.

Frontal cortex and hippocamp were the most intensely affected to the haloperidole and dexametasone in contrast with atypical antipsychotics (sulpiride, ziprasidone, olanzapine), presented significant lesser structural changes in frontal cortex and hippocamp.

The lots treated with dexametasone and sulpiride and dexametasone and ziprasidone are lesser affected at the cerebral structure level than the dexametasone and olanzapine treated lot.

Haloperidole has a significant decrease in neuroprotection.

Atipical antipsychotics demonstrated an neuroprotective effect.

The dexametasone animal model of stress is similar to the clinical model of schizophrenia evolution with multiple relapses in wich neuroprotection seems to be significantly altered.