title: Does maternal oxytocin protect the fetal brain?
abstract: By contrast to its inhibitory actions in adults, gamma-aminobutyric acid (GABA) is excitatory in the developing brain. The high intracellular chloride concentration [Cl(-)](i) in immature neurons causes a positive shift of the GABA(A) reversal potential so that opening of the GABA(A) channels results in depolarization due to chloride efflux. Because [Cl(-)](i) decreases during development, GABA becomes progressively inhibitory. A recent study has shown that a reduction in [Cl(-)](i) induced by endogenous oxytocin triggers a transient but profound switch of GABA actions from excitatory to inhibitory in the hippocampus of the rat fetus shortly before delivery and that this protects the fetal brain from hypoxic or hypoglycemic insult during delivery. The authors hypothesize that the oxytocin is derived from the maternal circulation, representing a novel form of communication between the brain of the mother and her offspring.
authors.affiliation: Centre for Neuroendocrinology and Department of Physiology, University of Otago, Dunedin 9012, New Zealand.
authors.forename: Colin H
authors.initials: CH
authors.lastname: Brown
authors.forename: David R
authors.initials: DR
authors.lastname: Grattan
mesh_terms: D000818:Animals; D001921:Brain / Q000196:embryology*; D019610:Cytoprotection / Q000502:physiology*; D005260:Female; D006801:Humans; D008431:Maternal-Fetal Exchange; D008564:Membrane Potentials / Q000187:drug effects; D010121:Oxytocin / Q000502:physiology*; D011247:Pregnancy; D011270:Pregnancy, Animal; D051381:Rats; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
chemical_list: D010121:Oxytocin; D005680:gamma-Aminobutyric Acid