Abstract
We tested the hypothesis that cortisol-induced release of fetal oxytocin triggers a perinatal inhibitory switch in γ-aminobutyric acid (GABA) signaling. The cortisol analog methylprednisolone did not modify GABA driving force and intracellular chloride concentration in 1-day-old rat hippocampal neurons. Together with the immaturity of the fetal rat hypothalamo-neurohypophysial system, these results suggest that oxytocin in the rat fetal brain is mainly provided by the mother.
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