Abstract
Many epidemiologic studies have documented a risk of schizophrenia with the appearance of maternal infection during pregnancy. Dysregulation of the brain development iduced by immune activation (overproduction of pro-inflammatory cytokines) has changed the program of neuronal apoptosis and synaptic pathology.
Animal model of perinatal infection was based on systemic administration of bacterial agens (endotoxin, lipopolysacharid, LPS) in a developmental period, which corresponds to the end of 2nd and main part of the 3rd trimester of human pregnancy. Male rat pups received LPS in dose 1mg/kg/day, i.p. during postnatal days 5.-9.
The rats were observed during an early postpubertal period in relation to persisting morphological damages and behaviour, exhibiting tight relationships to behavioural changes in schizophrenia (open field test, prepulse inhibition). LPS stimulation induced a mild growth retardation but no differences in other developmental milestones.
Young adult rats did not reveal any significant changes in the open field behaviour and brain histomorphology but prepulse inhibition was depressed. These findings document etiopathogenic importance of immune activation in neurodevelopmental aspects of schizophrenia.