Abstract
A risk of manifestation of schizophrenia can be correlated with the appearance of maternal and fetal infection during late pregnancy. Prolonged activation/dysfunction of microglia during brain development has long-lasting consequences for neuronal proliferation/cell death, which might be implicated among factors responsible for manifestation of schizophrenia.
Proposed model, induced by a systemic administration of bacterial endotoxin (lipopolysacharide, LPS) to rat pups in a developmental period corresponding to the end of 2nd and main part of the 3rd trimester of human pregnancy, will be used. The rats will be observed during an early postpubertal period and in adulthood as regards of assumed brain damage and numerical changes of microglial cells in a relationshp to hypofunction of glutamatergic system and schizophrenia-like behaviour.
Fiinal evaluation of these approaches will be aimed at etiopathological importance of neuroinfection in animal model based on the neurodevelopmental aspects of schizophrenia