Related Experiment Video
Updated: May 19, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
[Long-term cerebral effects of perinatal inflammation]
V Chhor1, A-L Schang, G Favrais
1Inserm U676, hôpital Robert-Debré, 48, boulevard Sérurier, 75019 Paris, France.
Abstract:
Perinatal inflammation can lead to fetal/neonatal inflammatory syndrome, a risk factor for brain lesions, especially in the white matter. Perinatal inflammation is associated with increased incidence of cerebral palsy in humans and animal models and there is a strong relationship with increased incidence of autism and schizophrenia in humans. Perinatal inflammation causes acute microglial and astroglial activation, blood-brain barrier dysfunction, and disrupts oligodendrocyte maturation leading to hypomyelination. Inflammation also sensitizes the brain to additional perinatal insults, including hypoxia-ischemia. Furthermore, long after the primary cause of inflammation has resolved, gliosis may also persist and predispose to neurodegenerative diseases including Alzheimer's and Parkinson's disease, but this relation is still hypothetical. Finding of acute and chronic changes in brain structure and function due to perinatal inflammation highlights the need for treatments. As gliosis appears to be involved in the acute and chronic effects of perinatal inflammation, modulating the glial phenotype may be an effective strategy to prevent damage to the brain.
Related Concept Videos
Bacterial Meningitis II: Pathophysiology
Cerebral Edema ll: Pathophysiology
Encephalitis ll: Pathophysiology
Chronic Inflammation: Introduction
Bacterial Meningitis I: Introduction

