Neonatal Proinflammatory Stress and Deficit of Induction of Long-Term Potentiation in the Hippocampus in Rats: Gender Differences

Abstract

The characteristics of long-term potentiation (LTP) in field CA1 of living hippocampal slices from rats aged 17–33 days were studied after neonatal administration of bacterial lipopolysaccharide (LPS) to evaluate the long-term effects of neuroinflammation in early ontogeny on synaptic plasticity. A deficit of LTP was seen in field CA1 of the hippocampus of rats surviving neonatal proinflammatory stress (NPS), the most sensitive being the mechanism of induction. In rats of the NPS group, synaptic potentiation was absent or weak in 61% of experiments, though when normal induction occurred, LTP persisted throughout the observation period. Correlation analysis showed that impairments to the development of the mechanisms of long-term plasticity in response to NPS are probably associated with weakening of the afferent influx to hippocampal neurons. Initially low-amplitude responses in field CA1 to application of single stimuli to Schaffer collaterals dominated in the hippocampus of female rats of the NPS group but were significantly rarer in males. This is probably why the early phase of potentiation in living hippocampal slices from females was virtually absent, though slow potentiation gradually developed. The hippocampus of males of the NPS group showed a statistically significant link between the effects of suppression of LTP and synaptic depression of initial potentials; signs of convulsive activity appeared when potentiation was successful. In contrast to males and the results obtained from all control groups, the hippocampus of female rats showed facilitation of the development of post-tetanic potentiation. It is suggested that this effect may be relevant to protective functions, which are evidently less effectively utilized in the hippocampus of males.