Related Experiment Video
Updated: Mar 20, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury
Julien Pansiot1, Hoa Pham2, Jeremie Dalous2
1Inserm, UMR1141, 75019 Paris, France; Université Paris Diderot, Faculté de Médecine, 75018 Paris, France; PremUP Foundation, 75014 Paris, France.
Insights
17β-estradiol (E2) protects neonatal rat brains from excitotoxic injury, a common cause of adverse neurodevelopmental outcomes in preterm infants. E2 influences glial cells, promoting white matter development and myelination.
Area of Science:
- Neuroscience
- Developmental Biology
- Neonatal Medicine
Background:
- White-matter injury in preterm infants leads to adverse neurodevelopmental outcomes.
- Limited interventions exist to prevent perinatal brain injury.
- 17β-estradiol (E2) shows neuroprotective potential but its role in developing glial cells requires further study.
Purpose of the Study:
- To investigate the neuroprotective effects of 17β-estradiol (E2) in a neonatal rat model of excitotoxic brain injury.
- To explore how E2 influences glial cell responses, specifically microglia and oligodendrocytes, in the developing brain.
Main Methods:
- Utilized an ibotenate-induced excitotoxic brain injury model in neonatal rats.
- Administered 17β-estradiol (E2) to assess its effects on cortical plate and white matter protection.
- Analyzed microglial phenotype balance and oligodendrocyte maturation in vivo and in vitro.
Main Results:
- E2 demonstrated significant neuroprotection in both the cortical plate and white matter.
- E2 modulated microglial phenotypes and accelerated oligodendrocyte maturation.
- Maturational effects of E2 on myelination were observed both in vivo and in vitro.
Conclusions:
- 17β-estradiol (E2) offers neuroprotection against neonatal excitotoxic brain injury.
- E2's effects on glial cell responses, including microglial modulation and oligodendrocyte maturation, underlie its neuroprotective properties.
- These findings suggest E2 as a potential therapeutic agent for preventing brain injury in preterm infants.
Abstract:
White-matter injury is the most common cause of the adverse neurodevelopmental outcomes observed in preterm infants. Only few options exist to prevent perinatal brain injury associated to preterm delivery. 17β-estradiol (E2) is the predominant estrogen in circulation and has been shown to be neuroprotective in vitro and in vivo. However, while E2 has been found to modulate inflammation in adult models of brain damage, how estrogens influence glial cells response in the developing brain needs further investigations. Using a model of ibotenate-induced brain injury, we have refined the effects of E2 in the developing brain. E2 provides significant neuroprotection both in the cortical plate and the white matter in neonatal rats subjected to excitotoxic insult mimicking white matter and cortical damages frequently observed in very preterm infants. E2 promotes significant changes in microglial phenotypes balance in response to brain injury and the acceleration of oligodendrocyte maturation. Maturational effects of E2 on myelination process were observed both in vivo and in vitro. Altogether, these data demonstrate that response of glial cells to E2 could be responsible for its neuroprotective properties in neonatal excitotoxic brain injury.
