Models of Perinatal Brain Injury in Premature and Term Newborns Resulting from Gestational Inflammation Due to Inactivated Group B Streptococcus (GBS), or Lipopolysaccharide (LPS) from E. coli and/or Immediately Postnatal Hypoxia-Ischemia (HI)

It is known that gestational and/or perinatal inflammation combined or not with hypoxia-ischemia (HI) is a risk factor for brain injuries, but the mechanisms underlying are still unclear. This chapter discusses about animal models mimicking those conditions, allowing scientists to uncover mechanisms involved and to study the adverse effects on the offspring. Here is presented a model of maternal inflammation induced by inactivated Group B Streptococcus (Sect. 2) and two experimental designs using LPS. One explores the effects of prenatal LPS administration and/or immediately postnatal HI (Sect. 3) and the second one, the immediately postnatal exposure to inflammation induced by LPS and/or HI (Sect. 4). For each animal model, the rationale supporting the model is exposed, followed by the procedures and the results obtained, allowing experimenter to reproduce and use these presented animal models.
Source: Springer protocols feed by Neuroscience - Category: Neuroscience Source Type: news