Effects of oxytocin on GABA signalling in the foetal brain during delivery
Rustem Khazipov1, Roman Tyzio, Yehezkel Ben-Ari
1INMED-INSERM U29, Université de la Méditerranée, Marseille, France.
Oxytocin (OXT) exerts multiple effects in the adult central nervous system. However, little is known about the effects of OXT on foetal neurons during delivery, at the time when a surge of OXT occurs. In a recent study, the effects of OXT on gamma-aminobutyric acid (GABA) signalling have been reported in foetal and newborn rats. In the immature rat hippocampal and neocortical neurons at birth, endogenous OXT induced a switch in the action of GABA from excitatory to inhibitory. This excitatory-to-inhibitory switch was caused by a switch in the polarity of the GABAergic responses from depolarizing to hyperpolarizing, reflecting a decrease in the intracellular chloride concentration. The effects of OXT were mimicked and occluded by bumetanide, a selective blocker of the chloride co-transporter NKCC1, suggesting that the effects of OXT involve inhibition of NKCC1. Neuronal death caused by anoxic-aglycaemic episodes was substantially delayed in the foetal hippocampus by endogenous OXT. These findings suggest that OXT plays important role in the preparation of the foetal brain to delivery.
Oxytocin (OXT) exerts multiple effects in the adult central nervous system. However, little is known about the effects of OXT on foetal neurons during delivery, at the time when a surge of OXT occurs. In a recent study, the effects of OXT on gamma-aminobutyric acid (GABA) signalling have been reported in foetal and newborn rats. In the immature rat hippocampal and neocortical neurons at birth, endogenous OXT induced a switch in the action of GABA from excitatory to inhibitory. This excitatory-to-inhibitory switch was caused by a switch in the polarity of the GABAergic responses from depolarizing to hyperpolarizing, reflecting a decrease in the intracellular chloride concentration. The effects of OXT were mimicked and occluded by bumetanide, a selective blocker of the chloride co-transporter NKCC1, suggesting that the effects of OXT involve inhibition of NKCC1. Neuronal death caused by anoxic-aglycaemic episodes was substantially delayed in the foetal hippocampus by endogenous OXT. These findings suggest that OXT plays important role in the preparation of the foetal brain to delivery.
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