Abstract
Neonatal inflammation produces long lasting alterations in the development and activity of neuroendocrine, immune and other physiological systems. We have recently reported administration of lipopolysaccharide (LPS) to neonatal female Wistar rats results in diminished follicular reserve and altered reproductive life span. Activation of the immune response has been suggested to underlie these effects, given the regulatory role of inflammation in reproductive functioning. Our current aim was to identify the cellular mechanisms that may underpin impaired ovulatory capacity and reduced oocyte development. On postnatal days (PNDs) 3 and 5 (birth = PND1) whole litters were treated with either 0.05 mg/kg of LPS (Salmonella Enteritidis) or an equivalent volume of non-pyrogenic saline. On PND 7 female pups were sacrificed and ovaries obtained. Microarray analysis revealed 712 genes were differentially regulated (2-fold change or greater; p
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