Abstract

Oxytocin is a neurohypophysal hormone known for its activity during labor and its role in lactation. However, the function of oxytocin (OTX) goes far beyond the peripheral regulation of reproduction, and the central effects of OTX have been extensively investigated, since it has been recognized to influence the learning and memory processes. OTX has also prominent effects on social behavior, anxiety, and autism. Interaction between glucocorticoids, OTX, and maternal behavior may have long-term effects on the developmental program of the developing brain subjected to adverse events during pre and perinatal periods. OTX treatment in humans improves many aspects of social cognition and behavior. Its effects on the hypothalamic–pituitary–adrenal axis and inflammation appear to be of interest in neonates because these properties may confer benefits when the perinatal brain has been subjected to injury. Indeed, early life inflammation and abnormal adrenal response to stress have been associated with an abnormal white matter development. Recent investigations demonstrated that OTX is involved in the modulation of microglial reactivity in the developing brain. This review recapitulates state-of-the art data supporting the hypothesis that the OTX system could be considered as an innovative candidate for neuroprotection, especially in the immature brain.

Highlights

  • Specialty section: This article was submitted to Pediatric Neurology, a section of the journal Frontiers in Neurology

  • Intrauterine growth restriction (IUGR) is a complication observed in 10% of the pregnancies [1] and represents the major causes of neonatal mortality and morbidity [2]

  • Placental insufficiency resulting in fetal hypoxia and maternal malnutrition are two identifiable and major causes of IUGR [3]

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Summary

Introduction

Specialty section: This article was submitted to Pediatric Neurology, a section of the journal Frontiers in Neurology. Interaction between glucocorticoids, OTX, and maternal behavior may have long-term effects on the developmental program of the developing brain subjected to adverse events during pre and perinatal periods. Clinical studies showed that abnormal inflammatory responses in the fetus and/or in the neonate can contribute to white matter damage [20, 21]. These clinical observations are well supported by studies conducted in rodents in which IUGR is associated with an abnormal neuroinflammatory response and myelinization defects [22,23,24], but is a risk factor for the development of inflammatory-induced brain damage [25]

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