A number of factors have been identified that appear to be associated with an increased risk of developing schizophrenia. Such factors as obstetric complications, viral infections, and early stressful experiences have been mimicked in animals in an attempt to understand their relationship to schizophrenia etiology (Lipska and Weinberger, 2000).
As in humans, gestational malnutrition (or prenatal protein deprivation) in rats results in severe and permanent changes in the development of the brain, as well as deficits in cognitive functioning and learning and abnormalities in neurotransmitter systems; some of these resemble changes found in schizophrenia.
Viruses have gained considerable attention as etiological factors in schizophrenia. A variety of viruses with the potential to infect the developing brain have been found to produce abnormalities in infected offspring similar to those observed in schizophrenia, long after the virus has cleared. For instance, prenatal exposure to the influenza virus has been shown to produce several neuroanatomical abnormalities including pyramidal cell disarray, reduced thickness of the neocortex and hippocampus, enlarged ventricles, as well as a significant reduction in cortical reelin expression. In utero infections in rats and mice with the lymphocytic choriomeningitis virus (LCMV) cause impairment of GABAergic neurons as well as excitatory amino acid neurotransmission. Exposure to the Borna disease virus produces abnormalities in the development of the hippocampus and neocortex. Prenatal infection with influenza appears to alter reelin in the brain.
Perinatal complications such as Cesarean birth and anoxia during birth in rats have been reported to produce changes in limbic dopamine function. However, these studies are difficult to interpret since C-sections alone seemed to produce more debilitating effects than C-sections with anoxia.
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