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Is oxytocin a maternal-foetal signalling molecule at birth? Implications for development
- Source :
- Journal of neuroendocrinology. 26(10)
- Publication Year :
- 2013
-
Abstract
- The neuropeptide oxytocin was first noted for its capacity to promote uterine contractions and facilitate delivery in mammals. The study of oxytocin has grown to include awareness that this peptide is a neuromodulator with broad effects throughout the body. Accumulating evidence suggests that oxytocin is a powerful signal to the foetus, helping to prepare the offspring for the extrauterine environment. Concurrently, the use of exogenous oxytocin or other drugs to manipulate labour has become common practice. The use of oxytocin to expedite labour and minimise blood loss improves both infant and maternal survival under some conditions. However, further investigations are needed to assess the developmental consequences of changes in oxytocin, such as those associated with pre-eclampsia or obstetric manipulations associated with birth. This review focuses on the role of endogenous and exogenous oxytocin as a neurochemical signal to the foetal nervous system. We also examine the possible developmental consequences, including those associated with autism spectrum disorder, that arise from exogenous oxytocin supplementation during labour.
- Subjects :
- Nervous system
endocrine system
medicine.medical_specialty
Offspring
Endocrinology, Diabetes and Metabolism
Neuropeptide
Biology
Oxytocin
Cellular and Molecular Neuroscience
Endocrinology
Neurochemical
Pregnancy
Internal medicine
medicine
Humans
Maternal-Fetal Exchange
reproductive and urinary physiology
Fetus
Endocrine and Autonomic Systems
medicine.disease
Signalling
medicine.anatomical_structure
Autism spectrum disorder
Female
hormones, hormone substitutes, and hormone antagonists
medicine.drug
Signal Transduction
Subjects
Details
- ISSN :
- 13652826
- Volume :
- 26
- Issue :
- 10
- Database :
- OpenAIRE
- Journal :
- Journal of neuroendocrinology
- Accession number :
- edsair.doi.dedup.....fad1f2abbcd54cfa55cd9452018de1df