Neonatal lipopolysaccharide induces pathological changes in parvalbumin immunoreactivity in the hippocampus of the rat.

Early exposure to infection is known to affect brain development and has been linked to an increased risk for schizophrenia. The present study aimed to determine whether neonatal infection produced long-term disruptions in behaviour and pathology that might provide a parallel with that observed in schizophrenia. Rats were administered lipopolysaccharide (LPS; 500 microg/kg i.p.) on postnatal day 7 and 9. Locomotor activity and object recognition memory were tested at day 35 and day 70. LPS animals were observed to be less active at adulthood as measured by locomotor activity. With regards to object recognition memory, LPS administration produced no early impairment in task performance, however, at day 70 LPS animals spent significantly less time exploring the novel object than control animals. Analysis of brains showed a reduction in expression of parvalbumin immunoreactive neurons in the hippocampus of LPS animals with significant reductions selectively localised to the CA1-CA3 region, and not the dentate gyrus. No changes were observed in prefrontal cortex. These results show that neonatal LPS results in pathophysiological brain changes in hippocampal CA1-CA3 subregions.